Oklahoma Heart Institute · tice, in patients with coronary heart dis-ease. 2,441 patients with a...

15th Annual Update in Cardiology Highlights

by Wayne N. Leimbach, Jr., MD

Metabolic Syndromeby Tobie L. Bresloff, MD

Atrial Flutterby David A. Sandler, MD

Oklahoma Hear t Inst i tutevolume 1 • number 2 • summer 2004

15th Annual Update in Cardiology Highlights

by Wayne N. Leimbach, Jr., MD



Oklahoma Hear t Inst i tute

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Edition 2

I n t h i s i s s u e

Letter from Dr. Leimbach 4

15th Annual Update in Cardiology

Highlights

Late Breaking Clinical Trials

By Wayne N. Leimbach, Jr., MD, FACC, FSCAI,FCCP, FAHA

5

Metabolic Syndrome

A Harbinger of Bad Things to Come

By Tobie L. Bresloff, MD

1 3

Atrial Flutter

New Treatment Strategies

By David A. Sandler, MD

2 6

Research Corner

Cardiovascular Research at Oklahoma Heart Institute

Cover photo by Rick Stiller

Tulsa from the Arkansas River by Day

2 9

3

OKLAHOMA HEART INSTITUTE AT UTICA

1265 S. Utica Avenue

Suite 300

Tulsa, OK 74104

Phone: 918.592.0999

Fax: 918.592.1021

OKLAHOMA HEART INSTITUTEAT SOUTHPOINTE

9228 S. Mingo

Suite 200

Tulsa, OK 74133

Phone: 918.592.0999

Fax: 918. 878.1021

THE DOCTORS OF OKLAHOMA HEART INSTITUTE

Wayne N. Leimbach, Jr., MD

Robert C. Sonnenschein, MD

Robert E. Lynch, MD

James J. Nemec, MD

John G. Ivanoff, MD

Gregory D. Johnsen, MD

Alan M. Kaneshige, MD

Ernest Pickering, DO

James A. Coman, MD

Edward T. Martin, MD

Roger D. Des Prez, MD

Christian S. Hanson, DO

Rebecca L. Smith, MD

Tobie L. Bresloff, MD

David A. Sandler, MD

Raj H. Chandwaney, MD

D. Erik Aspenson, MD

Frank J. Gaffney, MD

Yunus A. Moosa, MD

Tushar N. Shah, MD

4

TO OUR READERS:

Cardiology continues to be a rapidly evolving specialty with new technologies, new ther-

apeutic agents, and new treatment algorithms. We at Oklahoma Heart Institute find the

changes exciting and enjoy the challenge of keeping up to date.

Atrial flutter, a heart rhythm disorder that was once difficult to control, can now be treat-

ed very effectively. In this issue, Dr. David Sandler writes about some of the new ways to

conquer this problem.

Each year, Oklahoma Heart Institute Research and Education Foundation sponsors four

educational symposiums. The Winter Symposium, held in Las Vegas in February, concen-

trates on the subspecialty of electrophysiology. The Spring Symposium – Update In

Cardiology – focuses on general cardiology issues. The Summer Symposium, held this

year in July in Chicago, was devoted to Cardiovascular MRI. The Fall Nursing Symposium

highlights cardiology issues faced by nurses and other allied health professionals. This

issue of Oklahoma Heart Institute Magazine briefly summarizes some of the late breaking

clinical trials presented at this year’s 15th annual Spring Symposium.

In order to maximize the benefits of preventive cardiovascular medicine, Oklahoma

Heart Institute is pleased to expand our endocrine division with the addition of a third

endocrinologist. This summer, Dr. Erik Aspenson, a Board Certified endocrinologist,

joined Doctors Hanson and Bresloff in developing aggressive treatment algorithms for the

management of major risk factors for cardiovascular disease, including diabetes mellitus,

hyperlipidemia, hypertension and the dysmetabolic syndromes.

We are also pleased to announce the addition of three new cardiovascular subspecialists

to our team – Dr. Frank Gaffney and Dr. Tushar Shah, both noninvasive cardiologists and

Dr. Yunus Moosa, an interventional cardiologist. Now, with 20 doctors, our physician staff

can provide patients even better care.

We hope you enjoy the magazine and find it informative. We are interested in your com-

ments and suggestions.

Sincerely,

Wayne N. Leimbach, M.D.

Welcome to Oklahoma Hear tInst i tute Magazine

5

Advances in the field of cardiologycontinue to grow at a rapid pace. Theuse of large randomized double-blindclinical trials has accelerated the test-ing of new treatment strategies. Theseclinical trials are refining and improv-ing our ability to treat cardiovasculardisease. At the Oklahoma HeartResearch and Education Foundation’s15th Annual Update in Cardiology,highlights from significant late-break-ing clinical trials were presented anddiscussed.

The first two trials presentedaddressed the issue of how low LDLcholesterol levels should be lowered.It is important to remember that lovas-tatin, the first statin to be approved forlowering LDL cholesterol, wasapproved in 1987. In 1991 (13 yearsago), pravastatin and simvastatin wereapproved. At that time Sir MichaelOliver, a prominent researcher in thefield of lipid lowering, published an edi-

torial stating emphatically that “untilprimary prevention studies are com-plete, widespread use of hypolipidemicagents should be halted.” Since then,multiple large clinical trials havedemonstrated the benefit of loweringLDL cholesterol in both primary andsecondary prevention studies.

Two of the most recent trialsinclude the PROVE IT–TIMI-22 trial,which looked at whether intensive LDLlowering with atorvastatin producedgreater reductions in clinical eventsthan standard LDL cholesterol lower-ing with pravastatin, in patients pre-senting with acute coronary arterysyndromes. The other study, theALLIANCE Trial, was a comparison ofclinical outcomes in managed carepatients with coronary artery disease,treated with aggressive lipid loweringprograms using atorvastatin versus theusual care programs using a variety ofstatins.

The PROVE IT-TIMI-22 trial ques-tioned whether intensive LDL choles-terol lowering, to an average of lessthan 65mg/dl, achieves greater reduc-tions in clinical events than “standard”LDL lowering, to an average of95mg/dl. In this trial 4,162 patientswith acute coronary artery syndromewere treated with intensive standardmedical therapy and randomized toreceive either pravastatin 40m q hs oratorvastatin 80mg q hs. The primaryend point for this study was death, MI,documented unstable angina requiringhospitalization, revascularization orstroke. The median treatment LDLcholesterol for the pravastatin groupwas 95mg/dl; the median LDL choles-terol for the atorvastatin group was62mg/dl. Compared to the gold stan-dard treatment of lowering LDL choles-terol to less than 100mg/dl, the moreintensive lipid lowering strategy wasassociated with a 16% additional reduc-

15th Annual Update inCardiology Highlights

■ by Wayne N. Leimbach, Jr., MD, FACC, FSCAI, FCCP, FAHA

Late Breaking Clinical Trials

15th Annual Update inCardiology Highlights

• The early reduction in event rates in patients treated within 10days of an acute coronary syndrome event contrasts with anapproximately one to two year time lag seen in prior studies ofstatins (atorvastatin, lovastatin, pravastatin) in patients with chronicatherosclerosis (ASCOT, AFCAPS/TexCAPS, WOSCOPS, CARE,LIPID, PROSPER, 4S, HPS)TIMI 22 demonstrated that this acute coronary syndrome popula-tion, previously shown to have vulnerable plaques, can derive partic-ular benefit from early and intensive high-dose lipid lowering therapy• It cannot be determined from this study whether the long-termbenefit (2.5 years) was due to ongoing intensive lipid-lowering thera-py or the result of an early benefit in stabilizing vulnerable plaquesand limiting vascular remodeling with early and intensive treatmentfollowing the acute event• Ongoing double-blind, randomized, placebo-controlled trials suchas TNT, SEARCH and IDEAL, in patients with a history of CHD andchronic stable atherosclerosis will help to define the clinical benefitsof high-dose lipid lowering therapy in these populations

Events RatesEvents Rates

RR RR AtorvaAtorva 80 80 PravaPrava 4040

17%17% 1.9%1.9% 2.2% 2.2%

18%18% 6.3%6.3% 7.7% 7.7%

14%14% 12.2%12.2% 14.1% 14.1%

16%16% 22.4%22.4% 26.3% 26.3%

30 Days30 Days

90 Days90 Days

180 Days180 Days

End of Follow-upEnd of Follow-up

Primary Endpoint Over

Time

Primary Endpoint OverPrimary Endpoint Over

TimeTime

Atorvastatin 80mg Better

0.5 0.75 1.0 1.25 1.5Pravastatin 40mg Better

6

tion in risk of all causes of death ormajor cardiovascular events. Thereduction in relative risk of all causes ofmortality was even greater, at 28%, foratorvastatin versus pravastatin. Thisstudy, therefore, shows that there isadded benefit to further lowering LDLcholesterol by intensively treating highrisk patients. Interestingly, the benefitof the additional lipid lowering began at30 days and achieved statistical signifi-cance by 180 days. The benefit wasseen in all of the subgroups. There wasa mild increase in liver enzyme eleva-tions with more aggressive therapy.However, in the atorvastatin 80mggroup, only 3.3% had significant liverenzyme elevations.

The ALLIANCE study compared theclinical outcomes in managed carepatients with coronary heart disease,treated with aggressive lipid loweringusing atorvastatin versus usual care pro-grams using a variety of different statinmedications. This study was presentedat the American College of Cardiologymeeting in March, 2004 by Dr. DonaldB. Hunninghake from the University ofMinnesota. The background of thisstudy was that different lipid lowering

strategies have not been perspectivelystudied in real world settings. In addi-tion, physicians and patients have beenreluctant to use high dose statins due toperceived safety concerns. The hypoth-esis of the ALLIANCE study was thataggressive treatment of LDL cholesterolwith atorvastatin to below recommend-ed levels can provide incremental bene-fit, compared to standard clinical prac-tice, in patients with coronary heart dis-ease. 2,441 patients with a history ofcoronary artery disease were random-

ized to receive atorvastatin 10-80mg aday to get their LDL cholesterol below80mg/dl versus usual care to get theLDL cholesterol below 100mg/dl. TheLDL cholesterol levels changed from147 to 95 in the atorvastatin group ver-sus 147 to 111 in the usual care group.The primary end point for this studywas cardiac death, non-fatal MI, resusci-tative cardiac arrest, cardiac revascular-ization, or unstable angina requiringhospitalization. A 17% additional reduc-tion in cardiac mortality or majoradverse cardiac events and a 47% reduc-tion non-fatal MI’s was shown with themore aggressive lipid lowering strategy.In the atorvastatin group, liver enzymeelevations occurred in 0.7% of patientsin regards to the AST level and in 1.3%of patients in regards to the ALT levels.There were no documented cases ofrhabdomyolysis or myopathy. TheALLIANCE trial proved that aggressiveLDL lowering with atorvastatin, to lev-els lower than currently recommended,resulted in incremental clinical benefits,compared to usual care, without addi-tional safety concerns.

These two studies (PROVE IT-TIMI-22, and ALLIANCE) demonstrate signifi-cant additional reductions in cardiovas-cular risk by lowering LDL cholesterol

TIMI 22: Liver and

Muscle Effects

TIMI 22: Liver and

Muscle Effects

Strong inhibitors of CYP450 3A4 were excludedfrom the trial (due to atorvastatin metabolism)

Both drugs were generally well tolerated, and discontinuation

rates were similar for both agents

0.230.232.7%2.7%3.3%3.3%D/C for D/C for MyalgiaMyalgia/CK/CK

ElevationsElevations

0.240.241.1%1.1%1.5%1.5%CK > 3 ULNCK > 3 ULN

<0.001<0.0011.1%1.1%3.3%3.3%ALT > ULNALT > ULN

P-valueP-valuePravastatinPravastatin

40mg40mg

AtorvastatinAtorvastatin

80mg80mg

• For all randomizedpatients, the eventrates of the primaryendpoint at 2 yearswere 26.3%(537/2063) in thestandard dosepravastatin 40mggroup versus 22.4%(464/2099) in thehigh-dose atorvas-tatin 80mg group(p=0.005) represent-ing a 16% relativerisk reduction favor-ing high-dose ator-vastatin 80mg (CI,5%-26%)00 33 1818 2121 2424 2727 303066 99 1212 1515

TIMI 22 RESULTS: All-Cause Death or

Major CV Events in All Randomized

Subjects

TIMI 22 RESULTS: All-Cause Death or

Major CV Events in All Randomized

Subjects

%

with

Event

Months of Follow-up

PravastatinPravastatin 40mg40mg537/2063 (26.3%)537/2063 (26.3%)

AtorvastatinAtorvastatin 80mg80mg464/2099 (22.4%)464/2099 (22.4%)

16% RRR at 2 years16% RRR at 2 years

(p = 0.005)(p = 0.005)

3030

2525

2020

1515

1010

55

00

levels to below the currently recom-mended target levels. In addition,these benefits occurred without majorincreases in side effects. Physiciansshould, therefore, feel comfortablebeing more aggressive to lower LDLcholesterol levels in their patients.

The next late-breaking clinical trialto be presented was the VALIANTTrial. This study looked at the use ofan angiotensin receptor blocker, valsar-tan, as compared to an ace-inhibitor,captopril, for the treatment of patientswith left ventricular dysfunction postMI. The trial was to determinewhether valsartan was superior orequal to captopril, or whether a combi-nation of the two produced the bestoutcomes. 14,703 patients were ran-domized post MI to receive either cap-topril, with the maximum dose being

50mg tid, versus valsartan, the maxi-mum dose being 160mg bid, versus thecombination of the two. The studyfound there was no difference betweenthe treatment groups in regards tomortality. In addition, there was no dif-ference between the treatment groupsin regards to the combined endpoint ofcardiovascular death, non-fatal MI orheart failure. There was an increasedincidence of adverse side effects withcaptopril or the combination of capto-pril plus valsartan, as compared to val-sartan by itself. The conclusions werethat in patients with a myocardialinfarction complicated by heart failureand left ventricular dysfunction, orboth, valsartan was as effective as cap-

topril in reducing the risk ofdeath and in reducing the com-bined risk of cardiovasculardeath, non-fatal MI, or heartfailure. Therefore, based onthis study, it is felt thatangiotensin receptor blockerscan be used in place of ace-inhibitors where deemed appro-priate by the physician.

7

“Physicians shouldfeel comfortable being

more aggressive tolower LDL cholesterol

levels in theirpatients.”

©20

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orpo

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At Guidant, we’re pioneering

a new level of life-saving cardiac

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8

The SYNERGY Trial evaluated theuse of enoxaparin (low molecularweight heparin) versus unfractionatedheparin in 10,027 patients who present-ed with an acute coronary syndrome.These patients presented to the emer-gency room and were randomized toreceive enoxaparin 1mg/kg sub q ver-sus unfractionated heparin and werethen transferred to the catheterizationlaboratory for possible emergency per-cutaneous coronary interventions.The primary end point was death orMI at 30 days. This study found thatenoxaparin was not superior to unfrac-tionated heparin, but was as effective,and that the enoxaparin can be consid-

ered a safe and effective alternative tounfractionated heparin for patients athigh risk of acute coronary syndrome.Enoxaparin was, however, associatedwith a higher incidence of TIMI majorbleeding as compared to heparin.

The next two studies looked at anew drug that targets the endocannabi-

noid system to help smokers quitsmoking and help obese patients loseweight. The endocannabinoid systemis involved in the control of energy, bal-ance and body weight. It is alsoinvolved in the establishment of steadystate homeostasis for other neurotrans-mitters, mediators, hormones andcytokines. The endocannabinoid sys-tem exists in neurons of the mesolim-bic system which participates in rein-forcing reward and in translating moti-vation to action. Endocannaboidsinduce food intake after food depriva-tion. It is now known that nicotinestimulates the endocannabinoid recep-tors and repeated stimulation can lead

to self-administration of substanceabuse. Rimonabant is an endocannabi-noid receptor antagonist. The firststudy presented was the Reolipid study.In this study, obese patients were ran-domized between placebo and rimona-bant either 5mg or 20mg q day. The20mg dose of rimonabant produced a

weight loss of greater than 5% of base-line in almost 73% of patients. This rep-resented a major difference from place-bo. In regards to smoking cessation,rimonabant not only produced a 36%smoking abstinence rate, but also ledto weight loss in obese patients whoquit smoking. This represents a majorchange from the usual 10 poundweight gain seen in patients who quitsmoking in the placebo group.Rimonabant is currently not available,but is in clinical trials. It looks to be avery promising therapy for both smok-ing cessation and weight loss.

The SES-SMART trial looked at theproblems associated with high resteno-sis rates when treating small coronaryblood vessels with angioplasty andstents. In the past, bare metal stentsfailed to significantly reduce therestenosis rates seen with angioplastyprocedures. In this trial, patients wererandomized to receive either the newdrug-eluting stents versus the standardbare metal stents for treating smallcoronary blood vessels. At 8 months,restenosis rates were 9.8% for the drug-eluting group versus 53.1% for theangioplasty group. These results arevery encouraging and suggest thatmany patients referred for surgery

continued on Page 28

“These clinical trialsare refining andimproving our abilityto treat cardiovasculardisease . . .”

“These clinical trialsare refining andimproving our abilityto treat cardiovasculardisease . . .”

Since ACE inhibitors have been shown to reduce the risk of heart failure admis-sions and nonfatal MIs, as well as death, we compared the hazard ratios forthis composite event of the valsartan groups to the proven captopril regimen.The event rate for the valsartan monotherapy group was similar to captoprilwith a hazard ratio of 0.96. The combination of valsartan plus captopril wasalso no different than captopril alone with a hazard ratio of 0.97

Captopril

VALIANT TrialVALIANT Trial

CV Death, MI, or HF by TreatmentCV Death, MI, or HF by Treatment

Pfeffer, McMurray, Velazquez, et al. N Engl J Med 2003;349

Months

Valsartan vs. Captopril: HR = 0.96; P = 0.198

Valsartan + Captopril vs. Captopril: HR = 0.97; P = 0.369

0

0.1

0.2

0.3

0.4

0 6 12 18 24 30 36

Pro

bab

ilit

y o

f E

ven

t

Valsartan

Valsartan + Captopril

13

Articles about Metabolic Syndrome are becoming prevalentin the medical literature. Recently I was reading USAWeekend, in the Sunday Tulsa World, and there was an articletitled, “Do you suffer from Syndrome X? This deadly conditionleads to diabetes and heart disease.” The article goes on tocall Metabolic Syndrome the number 1 health problem inAmerica. You need to know more about this syndrome thanthe patients who are going to ask you questions.

Syndrome X was first described in 1988 by Dr. G.M.Reaven. It has also been called Reaven’s Syndrome, MetabolicSyndrome, Dysmetabolic Syndrome and Insulin ResistanceSyndrome. In 1998 the World Health Organization (WHO)published a working definition. This initial definition requiredan abnormality in handling glucose, or at least, insulin resist-ance plus 2 of four other factors. The more recent definitionfrom the National Cholesterol Education Program (NCEP)

which appears in the Adult Treatment Panel III (ATP III)Report is the most commonly used set of criteria. The crite-ria are listed in the table below. Three of the five listed valuesmust be met to make the diagnosis.

Recently there has been criticism that using three of thefive criteria might be too strict. The risk of cardiovascular dis-ease and diabetes goes up significantly with only 2 of the crite-ria being met.

Current estimates of the prevalence of Metabolic Syndromefigure that about 25% of all adults in America meet the criteria.This increases greatly with age, so that over age 60 the rate isbetween 40 and 45% of the population. According to the CDC,this also varies by ethnic background. Hispanics have thehighest prevalence, with non-Hispanic whites having amongthe lowest, and Native Americans as well as African Americansin the middle. This correlates inversely with insulin sensitivity

(how much a certain doseof insulin will bring bloodsugar down) in thesegroups. Whites are themost insulin sensitive, thenblacks, then Hispanics,who have the leastresponse to insulin.

The underlying defectthat is felt to be common topeople with MetabolicSyndrome is insulin resist-ance. This is defined byHaffner in Diabetes Care as“Impaired response to thephysiological effects ofinsulin (including those onglucose, lipid and proteinmetabolism) and theeffects on vascularendothelial function.” Thisis likely due to increasedvisceral fat as well as

MetabolicSyndrome

■ by Tobie L. Bresloff, MD

A Harbinger of BadThings to Come

NCEP ATP III Guidelines*:Identification Of The Metabolic Syndrome Positive Diagnosis Based on the Presence of 3 or More of the Following:

Defining LevelAbdominal Obesity(waist circumfrence)

Triglycerides

HDL Cholesterol

Blood Pressure

Fasting Glucose

Men >40 in (>102 cm)Women >35 in (>88cm)

<40 mg/dL

<50 mg/dL

Men 130/85 mm HgWomen 110 mg/dL (New level 100)

NCEP ATP III = National Cholesterol Education Program Adult Treatment Panel III. †Expert Panel on Detection,Evaluation, and Treatment of High Blood Cholesterol in Adults.http://www.nhlbi.nih.gov/guidelines/cholesterol/atglance.pdf

14

decreased activity level. The resistance then causes anincrease in insulin levels in the blood stream, and thishyperinsulinemia is felt to directly increase the factors thatcause cardiovascular disease. The final result is anincrease in diabetes mellitus, coronary heart disease,CVAs and mortality from all causes.How to make the diagnosis:

You can suspect Metabolic Syndrome if the patient isobviously overweight with the waist being the biggestpart. A family history of premature CAD or many relativeswith diabetes or lipid abnormalities should be clues, also.In addition, if a patient has hypertension, a lipid abnormali-ty or a hint of a glucose metabolism problem, you shouldget out the tape measure and see how big the waist actual-ly is, or calculate a BMI. You need a fasting lipid profile,not just a total cholesterol level. In addition, I suggest youcheck both a fasting glucose level, plus a 2 hour post-pran-dial blood sugar (after a normal lunch or a good sizedbreakfast) to look for impaired glucose tolerance (IGT). Ifyou only check fasting blood sugars, you will miss a signifi-cant number of people who have impaired glucose toler-ance as their only metabolic defect. This pre-diabetic stateshould be just as important in deciding risk as fasting glu-cose is. A normal HgA1c does not rule out MetabolicSyndrome.

Polycystic ovary disease and acanthosis nigricans are

also related to insulin resistance and are minor criteria thatpoint towards a diagnosis of Metabolic Syndrome. In addi-tion the WHO lists urinary microalbumin excretion ofgreater than 20 microgram/minute as a criterion.

Should Metabolic Syndrome be treated? I heardan expert say at a lecture that Food is the strongest drugand Exercise is the best diet. It would be great if we couldwrite a prescription for healthy diet and exercise and havethe pharmacist dispense it in a bottle. Instead, at the firstsign of Metabolic Syndrome, you should be urging thepatient to start a judicious diet to lose weight and make thebody more sensitive to insulin. This needs to be repeatedat each visit. A referral to a trusted dietician is also a goodidea. A diet with low glycemic index foods like theMediterranean diet will help. I have seen Type 2 diabetesmellitus go away entirely with a significant weight loss.Metabolic Syndrome patients can lessen their risk of devel-oping diabetes with only a 7-10% loss from their originalweight. They do not need to lose down to ideal weight toget benefit.

Patients always have reasons for not doing exercise. Orthey tell you how busy they keep with activities like knit-ting. (Knitting is actually better than just watching TV,since it is hard to eat while working 2 knitting needles, butthis is hardly exercise.) Exercise, at least every other day,

Identify metabolic syndrome and treat, if present, after

3 months of therapeutic lifestyle changes (TLC)

TLC Features

• TLC Diet:– Saturated fat <7% of calories, cholesterol <200 mg/day

– Consider increased viscous (soluble) fiber (10-25 g/day) and plant stanols/sterols (2g/day) astherapeutic options to enhance LDL lowering

• Weight management

• Increased physical activity

Treatment

• Treat underlying causes (overweight/obesity and physical inactivity):– Intensify weight management

– Increase physical activity

• Treat lipid and non-lipid risk factors if they persist despite these lifestyle therapies:– Treat hypertension

– Use aspirin for CHD patients to reduce prothrombotic state

– Treat elevated triglycerides and/or low HDL

NCEP ATP III = National Cholesterol Education Program Adult Treatment Panel III.

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults.

http://www.nhlbi.nih.gov/guidelines/cholesterol/atglance

continued on Page 25

SERVICES OF OKLAHOMA HEART INSTITUTE

Noninvasive Cardiology

• Nuclear Cardiology• Echocardiography & Doppler Studies• Nuclear and Echocardiographic

Exercise & Pharmacological StressTesting

• Transesophageal Echocardiography• Arterial Venous Peripheral Vascular

Imaging & Doppler Studies• Cardiovascular Magnetic Resonance

Imaging• External Counterpulsation (ECP)

Therapy

Invasive Cardiology

• Cardiac Catheterization• Coronary Angioplasty• Atherectomy• Rotablator Atherectomy• Thrombolytic Therapy• Coronary Stents• Intravascular Ultrasound• Myocardial Biopsy• Pericardiocentesis• Intravascular Radiation Therapy• Peripheral Angioplasty• Peripheral Stents

Metabolic Disorders

• Diabetes• Hypertension• Hyperlipidemia• Thyroid• Other Endocrine Problems

Electrophysiology

• Electrophysiology Studies• Ablation Therapy• Pacemaker Implantation• Pacemaker and Lead Extraction• Pacemaker Programming• Pacemaker Monitoring & Clinic• Implantable Cardioverter Defibrillator

(ICD) Placement• ICD Replacement• ICD and Hardware Removal• ICD Programming• ICD Monitoring and Clinic

• Holter Monitoring and Interpretation• 30 Day Cardiac Event Monitors• Implantation and Interpretation of

Long-term Heart Monitors• Signal Averaged EKGs and

Interpretation• Head Up Tilt Testing

and Interpretation• Direct Current Cardioversion• Antiarrhythmic Drug Loading and

Monitoring

Specialty Clinics

• Executive Health Clinic• Adolescent & Adult Congenital Heart

Clinic• Lipid & Wellness Clinic• Heart Failure Clinic• Dysrhythmia & Pacer Clinic

OKLAHOMA HEART INSTITUTEAT UTICA1265 S. Utica Avenue

Suite 300

Tulsa, OK 74104

Phone: 918.592.0999

Fax: 918.592.1021

OKLAHOMA HEART INSTITUTEAT SOUTHPOINTE9228 S. Mingo

Suite 200

Tulsa, OK 74133

Phone: 918.592.0999

Fax: 918. 878.1021

Wayne N. Leimbach, Jr.,MD, FACC, FSCAI,FCCP, FAHA

Dr. Leimbach isa subspecialist ininterventional car-diology, includingcardiac catheteri-zation, coronaryangioplasty andrelated interven-

tional procedures such as stents,atherectomy, laser, intravascular ultra-sound imaging and direct PTCA for acutemyocardial infarction. He is Director ofthe Cardiac and InterventionalLaboratories at Hillcrest Medical Center.Dr. Leimbach is Co-Director of the Lipidand Wellness Clinic at Oklahoma HeartInstitute. He is Director of the James D.Harvey Center for CardiovascularResearch at Hillcrest Medical Center, aswell as Director of the Oklahoma HeartResearch and Education Foundation. Healso serves as Clinical AssociateProfessor of Medicine at the Universityof Oklahoma College of Medicine –Tulsa. Dr. Leimbach completed a ClinicalCardiology Fellowship and a ResearchFellowship at the University of IowaHospitals and Clinics. He also completedhis Internal Medicine Internship andResidency programs at Iowa, where hewas selected Chief Resident in Medicine.He received his medical degree fromNorthwestern University in Chicago andhis Bachelor of Science degree from theUniversity of Michigan.

Board certified in Internal Medicine,Cardiovascular Disease andInterventional Cardiology

Robert C. Sonnenschein,MD, FACCDr. Sonnenscheinspecializes inechocardiographyand noninvasiveperipheral vascu-lar imaging. He isDirector ofPeripheralVascular

Ultrasound Imaging at Hillcrest MedicalCenter and Oklahoma Heart Institute andserves as Clinical Associate Professor ofMedicine at the University of OklahomaCollege of Medicine – Tulsa. He complet-ed hisCardiology Fellowship at the StateUniversity of New York Upstate MedicalCenter in Syracuse, where he also com-pleted his Internal Medicine Internshipand Residency programs. Dr.Sonnenschein received his medicaldegree from Rush Medical College inChicago and his Bachelor of Arts degreefrom the University of Pennsylvania.

Board certified in Internal Medicine,Cardiovascular Disease, and AdultEchocardiographyRegistered Vascular Technologist

Robert E. Lynch,MD, FACCDr. Lynch is a spe-cialist trained innoninvasive andinvasive cardiolo-gy. He is formerChief of Cardiology

at Hillcrest Medical Center, where healso has served as Chief of Medicine andPresident of the medical staff. Dr. Lynchis Co-Director of the Lipid and WellnessClinicat Oklahoma Heart Institute and Directorof the Executive Health Program. He isalso a Clinical Assistant Professor at theUniversity of Oklahoma College ofMedicine – Tulsa. Hecompleted his Cardiology Fellowship, aswell as his InternalMedicine Internship and Residency, atthe University of Oklahoma HealthSciences Center. Dr. Lynch received hismedical degree from the University ofOklahoma School of Medicine and hisBachelor of Science degree from theUniversity of Tulsa. Before establishinghis practice in Tulsa, he served as Chiefof Medicine at the U.S. Army Hospital,Bangkok, Thailand.

Board certified in Internal Medicine andCardiovascular Disease

James J. Nemec,MD, FACCDr. Nemec is asubspecialist inechocardiography,stress echocar-diog-raphy andnuclear cardiology.He serves asDirector ofNuclear Cardiology

for Oklahoma Heart Institute. Dr. Nemechas served as Assistant Professor ofInternal Medicine, Division of Cardiology,at Creighton University and as Assistant

T H E D O C T O R S O FO K L A H O M A H E A R T I N S T I T U T E

Professor, Department of Radiology, alsoat Creighton University. He completedhis Clinical Cardiology Fellowship at theCleveland Clinic Foundation and hisInternal Medicine Internship andResidency at Creighton University. Dr.Nemec also completed a year of trainingin pathology at the University ofMissouri, Columbia, MO. He received hismedical degree from CreightonUniversity, where he also received hisBachelor of Arts degree.


John G. Ivanoff,MD, FACC, FSCAIDr. Ivanoff spe-cializes in inter-ventionalcardiology, includ-ing cardiaccatheterization,coronary angio-plasty and relatedinterventional pro-

cedures such as stents,atherectomy and direct PTCA for acutemyocardial infarction. He is Director ofthe Catheterization Laboratories atSouthCrest Hospital. Dr. Ivanoff serves asClinical Associate Professor of Medicineat the University of Oklahoma College ofMedicine – Tulsa. He has also served asAssistant Professor of Medicine at theMedical College of Pennsylvania, as wellas Associate Director of the CoronaryCare Unit and Assistant Professor ofMedicine at Hahnemann UniversityHospital, where he also completed hisCardiology Fellowship. He completed hisInternal Medicine Internship andResidency at the Medical College ofPennsylvania, where he served as ChiefResident. Dr. Ivanoff also received hismedical degree from the Medical Collegeof Pennsylvania. He completed hisMasters degree in biochemistry atColumbia University and received hisBachelor of Arts degree from theUniversity of Pennsylvania.


Gregory D. Johnsen,MD, FACCDr. Johnsen is aninterventional car-diologist withexpertise in car-diac catheteriza-tion, angioplastyand related inter-ventional proce-dures, such as

stents and atherectomy. He is Director ofCardiac Rehabilitation at HillcrestMedical Center and Director of theHillcrest Exercise and LifestylePrograms. He completed his ClinicalCardiology Fellowship at the University ofOklahoma – Oklahoma City, where hethen finished an extra year of dedicatedtraining in interventional cardiology. Hecompleted his Internal MedicineInternship andResidency training at the University ofOklahoma – Oklahoma City, where healso received his medical degree. Dr.Johnsen received his Bachelor ofScience degree from Oklahoma StateUniversity.


Alan M. Kaneshige,MD, FACCDr. Kaneshige is anoninvasive cardi-ologist withexpertise in adultechocardiography,stress echocardio-graphy and trans-esophagealechocardiography.

He is Chief of Cardiology at HillcrestMedical Center. Dr. Kaneshige is also theDirector of the Adolescent and AdultCongenital Heart Clinic at OklahomaHeart Institute and Director of theCongestive Heart Failure C.A.R.E. Centerat Hillcrest Medical Center. Dr.Kaneshige completed his InternalMedicine Internship and Residency atCreighton University School of Medicine,where he also received his medicaldegree. He received a Bachelor ofScience in chemistry at CreightonUniversity. Dr. Kaneshige completed hisClinical Cardiology Fellowship atCreighton, where he also served as Chief

Cardiology Fellow for two years. He com-pleted an additional Cardiac UltrasoundFellowship at the Mayo Clinic inRochester, MN. Dr. Kaneshige served asAssistant Professor of Medicine atCreighton University School of Medicine,where he was Director of the NoninvasiveCardiovascular Imaging andHemodynamic Laboratory.

Board certified in Internal Medicine andCardiovascular DiseaseBoard certified in Adult andTransesophogeal Echocardiography

Ernest Pickering,DO, FACOIDr. Pickering is acardiology spe-cialist trained innoninvasive andinvasive cardiolo-gy with subspe-cialty expertise incardiac catheteri-zation and angio-

plasty. He is Chief of Cardiology atSouthCrest Hospital and past Chief ofCardiology at Tulsa Regional MedicalCenter. He completed a CardiovascularDisease Fellowship at Baylor College ofMedicine in Houston, TX. Dr.Pickering’s Internal MedicineResidency was completed at OklahomaOsteopathic Hospital in Tulsa. Hereceived his medical degree fromPhiladelphia College of OsteopathicMedicine and his Bachelor of Sciencedegree from Shelton College,Ringwood, NJ.


James A. Coman,MD, FACCDr. Coman is asubspecialist incardiacelectrophysiology,ablation therapyandpacemakers. He isDirector ofElectrophysiology

at Hillcrest Medical Center. Dr. Comanalso serves as Clinical AssociateProfessor of Medicine at the Universityof Oklahoma College of Medicine –Tulsa. He completed an

Electrophysiology Fellowship at theCleveland Clinic Foundation, where hewas Chief Fellow. His CardiologyFellowship was also performed at theCleveland Clinic Foundation. Dr. Coman’sInternal Medicine Internship andResidency training were completed atthe University of Alabama, Birmingham,AL. He received his medical degree fromthe University of Alabama School ofMedicine and his Bachelor of Sciencedegree in biomedical engineering fromVanderbilt University, Nashville, TN.

Board certified in Internal Medicine,Cardiovascular Disease andElectrophysiology

Edward T. Martin,MS, MD, FACC,FACP, FAHADr. Martin is anoninvasive cardi-ologist with sub-specialty expert-ise in non-inva-sive imaging. Heis Director ofCardiovascular

Magnetic Resonance Imaging atOklahoma Heart Institute, SouthCrestHospital and Hillcrest Medical Center.Dr. Martin is also Director of NuclearCardiology at SouthCrest Hospital. Inaddition, he is a Clinical AssociateProfessor of Medicine at the Universityof Oklahoma College of Medicine –Tulsa. Dr. Martin has specialty trainingin Nuclear Medicine, as well as addi-tional training dedicated toCardiovascular Magnetic ResonanceImaging. He completed his CardiologyFellowship at the University ofAlabama. Dr. Martin’s InternalMedicine Internship and Residencytraining were performed at TempleUniversity Hospital in Philadelphia. Hereceived his medical degree from theMedical College of Ohio. Dr. Martincompleted his Master of Sciencedegree in mechanical engineering atthe University of Cincinnati and hisBachelor of Science degree in physicsat Xavier University. Dr. Martin is afounding member of the Society ofCardiovascular Magnetic Resonanceand is an editorial board member ofthe Journal of Cardiovascular MagneticResonance.


Roger D. Des Prez,MD, FACCDr. Des Prez is anoninvasivecardiologist withsubspecialtyexpertisein echocardiogra-phy, nuclear cardi-ology and trans-esophageal

echocardiography. He is Director ofEchocardiography and PeripheralVascular Ultrasound Imaging atSouthCrest Hospital. Dr. Des Prezreceived his medical degree andBachelor of Arts degree from VanderbiltUniversity. He completed his Residencyin Internal Medicine and Pediatrics atUniversity Hospital of Cleveland. Dr. DesPrez practiced for six years as aninternist with the Indian Health Servicesin Gallup, NM. He returned to VanderbiltUniversity as a member of the InternalMedicine Faculty, at which time he alsocompleted his cardiology training. Inaddition to noninvasive cardiology, Dr.Des Prez is interested in outcomesresearch and computers in medicine.Board certified in Internal Medicine,Pediatrics, Critical Care andCardiovascular Disease

Board certified in Adult andTransesophageal Echocardiography

Christian S. Hanson,DO, FACEDr. Hanson is aspecialist inEndocrinology,Metabolism andHypertension atOklahoma HeartInstitutewithexpertise in dia-betes, lipids and

hypertension. He also serves as ClinicalAssociate Professor of Medicine in theCollege of Osteopathic Medicine –Oklahoma State University. He complet-ed a Fellowship in Endocrinology,Metabolism and Hypertension at theUniversity of Oklahoma in OklahomaCity. Dr. Hanson’s Internal MedicineResidency and Rotating Internship werecompleted at Tulsa Regional MedicalCenter. He received his medical degreefrom Oklahoma State University and hisBachelor of Science degree from orth-

eastern Oklahoma State University inTahlequah.

Board certified in Internal MedicineBoard certified in Endocrinology andMetabolic Diseases

Rebecca L. Smith,MDDr. Smith is anoninvasive cardi-ologist with sub-specialty expertisein transesophagealechocardiography,intra-operativeechocardiography,

stress and pharmacological echocardiog-raphy and contrast echo-cardiography.She completed an Advanced CardiacImaging Fellowship at the ClevelandClinic Foundation and her CardiologyFellowship at the University of NewMexico Health Sciences Center,Albuquerque, NM. Dr. Smith’s InternalMedicine Internship and Residency train-ing were performed at the University ofArizona Health Sciences Center inTucson. She received her medical degreefrom the Medical College of Ohio. Dr.Smith completed her Bachelor ofScience degree at Cleveland StateUniversity.

Tobie L. Bresloff,MDDr. Bresloff is aspecialist inEndocrinology,Metabolism andHypertension,with expertise indiabetes, lipids,hypertension and

thyroid diseases. She also serves asAssistant Professor in Clinical Medicineat the University of Oklahoma College ofMedicine - Tulsa. She completed an NIHFellowship in Endocrinology andMetabolism at Vanderbilt University inNashville, TN. Dr. Bresloff's InternalMedicine Internship and Residency werecompleted at Sinai Hospital of Detroit,Detroit, MI. She received her medicaldegree from Wayne State UniversitySchool of Medicine in Detroit and herMaster of Science and Bachelor ofScience degrees at the University ofMichigan, Ann Arbor, MI.

David A. Sandler, MDDr. Sandler is acardiologist withsubspecialtyexpertise in elec-trophysiology. Hecompleted hisCardiacElectrophysiologyFellowship and hisCardiovascular

Medicine Fellowship at New YorkUniversity Medical Center, New York, NY.Dr. Sandler's Internal MedicineInternship and Residency were per-formed at Mount Sinai Medical Center,New York, NY. He earned his medicaldegree from Georgetown UniversitySchool of Medicine in Washington, DC.Dr. Sandler received his Bachelor of Artsdegree at the University of Pennsylvaniain Philadelphia.

Board certified in Internal Medicine andCardiovascular DiseaseBoard certified in CardiacElectrophysiology

Raj H. Chandwaney,MD, FSCAIDr. Chandwaney isan interventionalcardiologist withexpertise in car-diaccatheterization,coronary angio-plasty and related

interventional procedures such as coro-nary stents, atherectomy, intravascularultrasound and peripheral vascular inter-ventional procedures. He completed hisClinical Cardiology Fellowship atNorthwestern University Medical Schoolin Chicago, IL., where he also completedan Interventional Cardiology Fellowship.Dr. Chandwaney's Internal MedicineInternship and Residency were per-formed at Baylor College of Medicine inHouston, TX. He received his medicaldegree from the University of Illinois atChicago. Dr. Chandwaney completed hisMaster of Science degree at theUniversity of Illinois at UrbanaChampaign, where he also received hisBachelor of Science degree.

Board certified in Internal Medicine andCardiovascular DiseaseBoard certified in InterventionalCardiology

D. Erik Aspenson,MD, FACE, FACPDr. Aspenson is asubspecialist inEndocrinology,Metabolism andHypertension atOklahoma HeartInstitute, withexpertise in dia-betes,

lipids, hypertension and thyroid diseases.He completed a Fellowship inEndocrinology at Wilford Hall MedicalCenter, Lackland AFB, Texas. Dr.Aspenson's Internal Medicine Internshipand Residency were completed at DavidGrant Medical Center, Travis AFB,California where he served as ChiefResident. He received his medicaldegree from the University of Oklahomaand his Bachelor of Science degree atOklahoma State University.

Board certified in Internal MedicineBoard certified in Endocrinology andMetabolic Diseases

Frank J. Gaffney, MDDr. Gaffney is aninvasive and non-invasive cardiolo-gist with subspe-cialty expertise intransesophagealechocardiography.He completed hisCardiovascularMedicine

Fellowship at Scott & White MemorialHospital in Temple, Texas. Dr. Gaffneycompleted his Internal MedicineInternship and Residency at BrookeArmy Medical Center in San Antonio. Hethen remained on staff at Scott & WhiteMemorial Hospital for several years,before entering his Fellowship inCardiovascular Medicine. Dr. Gaffneyearned his medical degree from NewYork Medical College, Valhalla, NewYork, and he received his Bachelor ofArts degree at Hofstra University inHempstead, New York.

Board certified in Internal MedicineBoard eligible in Cardiovascular Disease

Yunus A. Moosa,MD, FACC, FACP,FSCAIDr. Moosa is aninterventional car-diologist withexpertise in car-diac catheteriza-tion, coronaryangioplasty andrelated interven-

tional procedures such as coronarystents, atherectomy, intravascular ultra-sound and peripheral vascular interven-tional procedures. He completed hisClinical Cardiology Fellowship at HowardUniversity in Washington, DC, where healso completed his Internal MedicineInternship and Residency. Dr. Moosareceived his medical degree from theUniversity of Ibadan, Nigeria. Heobtained his Bachelor of Science degreeat the University of Durban-Westville,South Africa.

Board certified in Internal Medicine andCardiovascular DiseaseBoard certified in InterventionalCardiology

Tushar N. Shah, MDDr. Shah is a non-invasive cardiolo-gist with a sub-specialization incardiac imaging.He has advancedtraining in adultand tranesophagealechocardiography,

nuclear cardiology, cardiac CT, and vas-cular imaging. He completed hisCardiology Fellowship at BaylorUniversity Medical Center in Dallas,Texas, where he was Chief Fellow for twoyears. Dr. Shah completed his InternalMedicine training at Duke UniversityMedical Center in Durham, NorthCarolina. He received his medical degreewith highest honors from the Universityof North Carolina in Chapel Hill and hisBachelor of Arts degree from theUniversity of Pennsylvania inPhiladelphia.

Board certified in Internal Medicine andCardiovascular DiseaseBoard certified in Adult andTransesophageal EchocardiographyBoard certified in Nuclear Cardiology

20

Peace of Mind.

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Peace of Mind.• Stark • Antikickback • HIPAA• Shareholder and Employment

Agreements• Sale of Practice • Medicare• Physician contract review• Hospital medical staffs• Audits & recoupments

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• Estate planning and probate • Tax planning• Retirement plan design and consulting• Corporate and business law• Contracts • Real estate • Securities

Johnson, Jones, Dornblaser, Coffman & Shorb, P.C.proudly representing Oklahoma Heart Institute since its inception

E. Andrew Johnson, attorney-at-law15 W. Sixth Street, Suite 2200 • Tulsa, OK 74119 • (918) 584-6644 • [email protected]

This magazine serves as a majorcommunication source for

Oklahoma Heart Institute, pro-viding physicians and their

patients throughoutNortheastern Oklahoma with

important information.

If you would like to becomea co-sponsor call LauraNorris at 1.800.561.4686

or [email protected]

15th Annual Update in Cardiology Highlightsby Wayne N. Leimbach, Jr., MD



Oklahoma Hear t Inst i tutevolume 1 • number 2 • summer 2004

15th Annual Update in Cardiology Highlightsby Wayne N. Leimbach, Jr., MD



Oklahoma Hear t Inst i tute

Oklahoma Hear tInstitute

Thankyou!

to all our co-sponsors for helping to make our magazine a success.

Publishing Concepts, Inc.14109 Taylor Loop Road

Little Rock, AR 72223501.221.9986 / 800.561.4686

25

even without weight loss, will partiallyhelp to overcome insulin resistance.There must be something each patientcan do. An inexpensive pedometer tocount their steps can be a good motiva-tor. You just need to keep mentioningthat exercise is cheap, and has no sideeffects like so many medicines do.

We know that many patients neverdo lose weight, or become more active.Then we need to talk about medica-tions. There are no medicines approvedfor use for Metabolic Syndrome. Thereare oral hypoglycemic agents that helpsensitize the body to insulin, but theseare only indicated for use in diabetes.These drugs appear to look promising,but there are no studies yet concludedto show if they should be recommend-ed. We can, however, treat the individ-ual risk factors individually and aggres-sively. In a hypertensive, treat with anACE inhibitor, or an ARB. These aremore expensive, but are better at pre-venting microalbuminuria and protect-ing the kidneys. For dyslipidemia, treatto the goals of the ADA with a statinand/or niacin for the triglycerides. Alsouse aspirin to reduce platelet aggrega-tion and decrease the inflammatoryresponse that leads to atherosclerosis.

Metabolic Syndrome needs to belooked for, tested for, and treated withthe appropriate medications plus thenever-ending reminders about diet andexercise. Making the patient informedabout the risks helps. There are goodpatient handouts on both the ADA andthe AHA web sites.

Helpful web sites:

American Diabetes Association “Standards of Medical Care in Diabetes”

http://care.diabetesjournals.org/content/vol27/suppl_1/#POSITION_STATEMENTSGlycemic index:

http://www.diabetes.org/diabetes-forecast/apr2003/research.jspADA Patient handout on Metabolic Syndrome:

http://www.diabetes.org/weightloss-and-exercise/weightloss/metabolicsyndrome.jspAmerican Heart Association Patient handout:

http://www.americanheart.org/presenter.jhtml?identifier=4756AHA Definition of Metabolic Syndrome and treatment recommendations:

http://circ.ahajournals.org/cgi/content/full/109/3/433

Therapeutic Lifestyle Changes (TLC)

TLC Features

• TLC Diet:– Saturated fat <7% of calories, cholesterol <200

mg/day

– Consider increased viscous (soluble) fiber (10-25g/day) and plant stanols/sterols (2g/day) astherapeutic options to enhance LDL lowering

• Weight management

• Increased physical activity




continued from Page 14

Identify metabolic syndrome and treat, if present, after

3 months of therapeutic lifestyle changes (TLC)

Treatment

• Treat underlying causes (overweight/obesity andphysical inactivity):– Intensify weight management

– Increase physical activity

• Treat lipid and non-lipid risk factors if they persist despitethese lifestyle therapies:– Treat hypertension

– Use aspirin for CHD patients to reduce prothrombotic state

– Treat elevated triglycerides and/or low HDL




Atrial flutter is perhaps the most well described heart rhythmdisorder, and its treatment is an excellent example of theprogress of modern medicine. Through advances in science andtechnology we have developed ways to conquer a disorder thatwas once difficult to control.

Atrial flutter was first described by its “sawtooth” electrocar-diographic appearance in 1911. Amazingly, as early as 1920, SirThomas Lewis envisioned the mechanism of this arrhythmia tobe circus movement in the right atrium. However, it was notuntil the development of clinical electrophysiology in the 1970s,that we solidified our understanding of this arrhythmia. We nowrecognize that electrical activation in typical atrial flutter is acounter-clockwise reentrant circuit within the right atrium, cir-cling the tricuspid valve (Figure 1). Importantly, there is aregion of slowed conduction between the inferior vena cava andthe tricuspid valve that is critical to arrhythmia propagation. It isthis area that is targeted in ablation.

In order to properly diagnose typical atrial flutter, it is impor-tant to analyze the morphology of the flutter waves on a 12-leadelectrocardiogram. Downward flutter waves in leads II, III andaVF with pointed, upward P waves in V1 are diagnostic of typicalatrial flutter (Figure 2). Upward P waves in V1 – even at regularintervals – are seen commonly in atrial fibrillation and do notalone diagnose atrial flutter. Although often recognized easily,atrial flutter can occasionally be missed if rapid conductionobscures every other flutter wave, as seen with 2:1 conduction.

Recent population studies have shown that atrial flutter is acommon arrhythmia, affecting 88 people in every 100,000. Ofgreat importance is that the risk of stroke appears to be similarto that in patients with atrial fibrillation. Until the developmentof radiofrequency ablation, therapies for atrial flutter were limit-ed and generally ineffective. With cardioversion alone, the six-month recurrence rate is 55%. Even with anti-arrhythmic med-ications, long-term recurrence is 60%.

In the 1980s, catheter ablation procedures revolutionized thetreatment of atrial flutter. Because conduction through theregion between the inferior vena cava and tricuspid valve(cavotricuspid isthmus) is critical to arrhythmia propagation, itwas hypothesized that destroying this tissue would terminate thearrhythmia. More importantly, eradicating conduction in thisarea would eliminate the substrate for recurrence.

Because of its effectiveness, ablation for atrial flutter has

become commonplace. In our laboratory, the procedureinvolves placement of electrical catheters through the rightfemoral vein. The catheters are then positioned in various loca-tions within the right atrium and right ventricle. One catheter isplaced in the region of the cavotricuspid isthmus and radiofre-quency energy is applied. A line is created from the tricuspidvalve to the inferiorvena cava (Figure 3).

Initially, the end-point of ablation ofatrial flutter was termi-nation of the tachycar-dia. However, thisapproach had twomajor drawbacks.This approachrequired the presenceof the arrhythmia atthe time of the proce-dure and was fraughtwith a significantrecurrence rate. Thecurrent endpoint ofthe procedure isdevelopment of con-

■ by David A. Sandler, MD

26

Atrial Flutter

New Treatment Strategies

Figure 1. Mechanism of typical atrial flut-ter. The critical area between the inferiorvena cava and the tricuspid valve isshown in yellow. (Morady F NEJM1999;340(7):534-43)

Figure 2. Electrocardiogram of typical atrial flutter

duction block across the cavotricuspid isth-mus. Because this endpoint does notrequire the presence of atrial flutter, theprocedure may be performed in normalsinus rhythm. Another benefit of thisapproach is a very low rate of recurrence.The duration of the entire procedure is usu-ally less than one hour.

In contrast to the poor success of anti-arrhythmic therapy, ablationcarries a success rate greater than 95%. The complication rate of thisprocedure is remarkably low, under 1%. Typical complications arethose associated with femoral venous access, such as hematoma,bleeding and deep venous thrombosis. Major complications, such asstroke, AV block, pericardial tamponade and pulmonary embolism,are extremely rare.

Clearly, ablation procedures have dramatically improved the man-agement of atrial flutter, but should ablation be a first-line therapy?As seen in Figure 4, the risk of hospitalization or developing atrial fib-rillation at two years is lower with ablation than with anti-arrhythmictherapy. Furthermore, ablation confers a higher likelihood of main-taining normal sinus rhythm.

If there is an Achilles’ heel to ablation of atrial flutter, it is thedevelopment of atrial fibrillation. Although atrial flutter can occur inthe absence of heart disease, many patients with atrial flutter haveconcomitant congestive heart failure, hypertension and coronaryartery disease. As one would expect, it is these risk factors that pre-dict the development of atrial fibrillation. Also intuitively, the pres-ence of prior atrial fibrillation predicts development of atrial fibrilla-tion after atrial flutter ablation. This is shown in Figure 5.

Applying these concepts, patients at high risk of developing atrialfibrillation should generally be treated medically. Patients at low tomedium risk of developing atrial fibrillation should be targeted forflutter ablation, even as a first-line therapy. After ablation, mostpatients should be treated aggressively for prevention of atrial fibrilla-tion with ACE inhibitors and beta-blockers. Anti-coagulation shouldbe guided by the same principles that apply for atrial fibrillation.

The understanding and management of atrial flutter haveadvanced significantly since its description almost a century ago. Wenow can identify and cure patients with atrial flutter readily withradiofrequency ablation. The efficacy and safety profile of ablation isfar superior to anti-arrhythmic therapy alone.

Figure 3. Left anterioroblique (LAO) and right ante-rior oblique (RAO) fluoroscop-ic views of atrial flutter abla-tion. (RA = right atrium, LA =left atrium, RV = right ventri-cle)

Figure 4. Ablation versusanti-arrhythmic therapy as afirst line therapy for atrial flut-ter. (Natale A, Newby KH,Pisanó N, et al. J Am CollCardiol 2000;35:1898 –904)

Figure 5. Risk of developingatrial fibrillation after radiofre-quency ablation of atrial flut-ter (Paydak H, Kall JG,Burke MC, et al. Circulation1998;98(4):315-22)

27

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because of small vessels can now betreated in the catheterization laboratorywith angioplasty and drug-eluting stents.

The SCD-HeFT trial compared amio-darone treatment with conservativelyprogrammed shock-only implantabledefibrillators. The study showed virtual-ly no benefit was derived from the amio-darone therapy, whereas even the con-servative shock-only ICDs were benefi-cial. The DINAMIT trial was a random-ized trial testing prophylactic implantabledefibrillator therapy against optimal med-ical management early after myocardialinfarction. There was a highly significantreduction in dysrhythmic deaths in theimplantable cardiac defibrillator group.These trials continue to show the bene-fits of cardiac implantable defibrillators.

The late breaking clinical trials thisyear demonstrate the accelerating paceof treating and preventing cardiovasculardiseases. Aggressive lowering of LDLcholesterol produces significant benefitswithin just a couple years. Angiotensinreceptor blockers can be used instead oface-inhibitors for the treatment of leftventricular dysfunction post MI.Unfractionated heparin and low molecu-lar weight heparin can be used inter-changeably for patients taken to thecatheterization laboratory for percuta-neous coronary interventional proce-dures. There is significant value ofimplantable cardiac defibrillators in pre-venting sudden cardiac death. Finally,the new class of agents to block theendocannabinoid receptors may showsubstantial benefit for the treatment ofobesity and smoking addiction.

28

continued from Page 8©

2003

Gui

dant

Cor

pora

tion

w w w . g u i d a n t . c o m

Bob had a Guidant defibrillator implanted in 2001

At Guidant, we’re pioneering

a new level of life-saving cardiac

and vascular technology to give

patients another day. Another

year. Another lifetime. Guidant is

proud to support the Oklahoma

Heart Institute.

We believe every day is worth living.

“The late breaking clinicaltrials this year demonstrate

the accelerating pace oftreating and preventing

cardiovascular diseases.”

RimonabantRimonabant

20mg (%)20mg (%)RimonabantRimonabant 5 5

mg (%)mg (%) Placebo Placebo

(%) (%)

72.9 **72.9 **41.8 *41.8 *27.627.6Weight Loss of >Weight Loss of >

5% of Baseline5% of Baseline

PtPt’’s on Rxs on Rx

for 1 year for 1 year

44.344.316.316.310.310.3Weight Loss of >Weight Loss of >

10% of Baseline10% of Baseline

PtPt’’s on Rxs on Rx

for 1 yearfor 1 year

RimonabantRimonabant

10mg (%)10mg (%)RimonabantRimonabant 5 5

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GroupGroup

*=p0.01: **=p<0.001 vs placebo

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main: 918.624.97192way: [email protected]: 918.624.9798fax: 918.261.1050

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RESEARCH CORNER

Through the Oklahoma Heart Institute Researchand Education Foundation, Oklahoma Heart Institutedoctors have been involved in clinical research stud-ies for the past 15 years. The research conducted byOklahoma Heart Institute includes studies on hyper-tension, acute myocardial infarction, unstable angina,congestive heart failure, angiogenesis, hyperlipi-demia, diabetes mellitus, and dysrhythmias.Oklahoma Heart Institute has also been engaged inresearch involving new devices such as stents, pace-makers, implantable cardiac defibrillators, bi-ventricu-lar pacemakers for the treatment of heart failure, andintravascular imaging devices. In addition, new imag-ing techniques involving nuclear medicine imaging,as well as cardiovascular MRI imaging, have beencarried out.

Oklahoma Heart Institute participates in clinicalresearch trials to provide patients with the newesttreatment strategies, as much as several years priorto FDA approval and normal clinical availability.Additionally, the research studies provide training andexpertise in new therapies for both physicians and themedical staff working with them. Oklahoma HeartInstitute employs seven research nurses; three areinvolved with inpatient studies and four with outpa-tient studies. Outpatient research includes studies ontreatment strategies for patients with hyperlipidemia,hypertension, diabetes mellitus, and heart failure.Many studies start with patients while they are in thehospital. These are referred to as inpatient trials.

The FINESSE trial looks at different treatmentstrategies for patients presenting with an acutemyocardial infarction, analyzing the use of throm-bolytic therapy prior to emergency catheterizationand primary angioplasty versus primary angioplasty

without pre-cath thrombolytic therapy. The goal ofthe FINESSE trial is to determine whether the bene-fits of earlier reperfusion with thrombolytic therapyoutweigh the potential bleeding risk of thrombolytictherapy, as compared to primary angioplasty by itself.The ACUITY trial compares different anticoagulationstrategies with primary angioplasty in the setting ofacute coronary artery syndromes by examining therelative value of low molecular weight heparin versusstandard heparin therapy versus angiomax(bivalirudin).

The HAT trial studies the use of home defibrilla-tors for patients post anterior wall myocardial infarc-tion who do not meet the criteria for implantable car-diac defibrillators. The PERISCOPE Trial comparestwo types of diabetic medicines to see whether or notthere is less progression of atherosclerotic coronaryartery disease and, possibly, more regression of coro-nary artery disease with P PAR agonists versus stan-dard hypoglycemic agents. This investigation is anintravascular ultrasound study similar to the REVER-SAL Trial, which recently demonstrated that coronaryartery disease regression can occur within 18 monthswith aggressive lipid lowering.

Another intravascular ultrasound guided study ran-domized patients between Lipitor versus Lipitor plustorcetrapib. This trial looks at the use of a statin tolower LDL versus the combination of statin therapyplus an HDL-cholesterol raising medicine to evaluatewhether significant regression can occur in less thantwo years with the combination of Lipitor plus torce-trapib.

The A-HeFT study looks at a hydralazine Isordilcombination pill versus placebo in African Americanpatients having New York Heart Association class III

CARDIOVASCULAR RESEARCH AT OKLAHOMA HEART INSTITUTE

30

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and IV heart failure. This investigation compares thenew medication to the current standard therapy ofACE inhibitors, diuretics and beta blockers. Patientsare randomized to the new hydralazine Isordil combi-nation plus standard therapy versus placebo plus stan-dard therapy. There are preliminary studies suggest-ing that the addition of hydralazine plus nitrates maybe particularly beneficial to African Americans withheart failure.

The SALT-II trial looks at a new class of medicineinvolving the inhibition of vasopressin. This studyuses Tolvaptan for the treatment of hyponatremia.Patients with serum sodium of 134 or less are eligiblefor this study.

The Carperatide IV study for heart failure analyzesthe value of an atrial naturetic peptide when given asan intravenous infusion in patients with severe heartfailure.

Several trials currently being performed examinethe use of biventricular pacemakers and implantablecardiac defibrillators. In addition, drug studies fordysrhythmias are also being performed. Theseinclude studies on Azimilide for the treatment of atrialdysrhythmias, as well as a study called the SHIELDTrial, evaluating the use of Azimilide to decrease theepisodes of implantable cardiac defibrillator firings inpatients.

The recently completed PREVAIL Trial looked at anew class of antioxidants for the prevention ofrestenosis following coronary artery stent placement.

Oklahoma Heart Institute has been involved inmany landmark trials over the years, including therecently published REVERSAL trial, investigating theuse of intravascular ultrasound to demonstrate thevalue of very aggressive cholesterol lowering. In thisstudy, Lipitor 80mg a day was used in patients tolower LDL cholesterol significantly below currentlyrecommended target levels, demonstrating that pro-gression can be stopped within 18 months by very

aggressive cholesterol lowering. In addition, manypatients demonstrated actual plaque regression within18 months as evidenced by intravascular ultrasoundstudies. Oklahoma Heart also participated in suchtrials as the CARE Trial, which confirmed the value ofsecondary prevention with the use of statins.

Oklahoma Heart Institute was involved in theSAVE Trial, which demonstrated the benefit of ACEinhibitors for the prevention of heart failure post MI.The VALIANT Trial was a similar trial, showing thevalue of angiotensin receptor blockers in patients withLV dysfunction post MI.

Physicians with patients who might be interestedin participating in clinical research trials can contactOklahoma Heart Institute to obtain details on current-ly enrolling studies. Physicians may also inquireabout new therapies not clinically available to the pub-lic outside of research studies. These have been par-ticularly helpful for patients for whom there is cur-rently no good clinical therapy.

The past 15 years have been very exciting inregards to clinical and technical advances in the fieldof cardiology. The physicians at Oklahoma HeartInstitute are very optimistic about even more excitingadvances that will be made over the next 5-10 years.

Oklahoma Heart participates in 20-40 research tri-als at any given time. Studies can last from a few daysfor up to five-six years.

For further details of the research studies beingconducted at Oklahoma Heart Institute, please call592-0999 and ask for one of the research nurses.

RESEARCH CORNER

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7the life of someone is improved bya Medtronic product or therapy.

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This magazine serves as amajor communication

source for Oklahoma HeartInstitute, providing physicians and their patients throughout

Northeastern Oklahomawith important information.

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call Laura Norris at1.800.561.4686

or [email protected]

Treating Hypercholesterolemiaby Wayne N. Leimbach, Jr., MD

Implantable Defibrillators Clearly Lifesaversby James A. Coman, Jr., MD

A Sharper Cardiac Imageby Edward T. Martin, MD

The Executive Health Program at Oklahoma Heart Instituteby Robert E. Lynch, MD

Oklahoma Heart Inst i tutevolume 1 • number 1 • winter 2004Welcome to

OklahomaHeart

InstituteMagazine

Avid athletes and tennis players, Denise and Norma could be quite the doubles team. But when cardiacproblems slammed the ball in their court, they turned to SouthCrest for the ultimate save.

SouthCrest Hospital is dedicated to innovative cardiac care. With an entire floor designed for heartpatients – complete with thirty-two all-private rooms – a low patient-to-nurse ratio and a beautifulcomfortable environment, we provide the right conditions for recovery.

Now, Denise and Norma take care of their hearts and playby a new set of rules. With all the improvements thatSouthCrest brings to cardiac care, you’ll see that we takeinnovation to heart.

What brought you to SouthCrest – Tulsa’s Heart Hospital?

w w w . s o u t h c r e s t h o s p i t a l . c o m / 9 1 8 - 2 9 4 - 4 0 0 0

L O C A T E D A T H I G H W A Y 1 6 9 & 9 1 s t S T R E E T

W E T A K E i n n o v a t i o n T O H E A R T

NORMA DUKE

Mother of Denise,grandmother of nine.

Lifelong tennis player.

Experienced chest pains,went to family doctor.

Stress test revealed 95%blockage in an artery.

Now, she’s back in theswing after angioplasty and stent implantation at SouthCrest.

DENISEWESTFALL

Daughter of Norma.

Director of the swimmingprogram at Jenks.

Gave her mom a cardiac stress test, but mom gave it back.

Denise was diagnosedwith cardiomyopathy.

Takes medicine, exercises,is getting along swimmingly.

OKLAHOMA HEART INSTITUTE1265 S. Utica AvenueSuite 300Tulsa, OK 74104

Presorted StandardU.S. POSTAGE PAID

Little Rock, ARPermit No. 2437

Oklahoma Heart Institute · tice, in patients with coronary heart dis-ease. 2,441 patients with a...

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