By Louis Kuritzky, MD
Screening for Hypertrophic Cardiomyopathy
Although death in young athletes is an uncommon problem, hypertrophic cardiomyopathy (HC) remains one of the more frequent etiologies, responsible for up to one-third of all U.S. fatalities prior to age 35. Since 1971, Italy has required annual preparticipation sports examinations, which includes EKG, limited exercise testing, and other traditional screening evaluations. Additionally, if screening history or physical so indicated, echocardiography was performed.
Of 33,735 screened athletes, 8.9% were referred for echocardiography because of suspicious history, physical, or EKG findings. Twenty-two athletes were determined to have HC and subsequently disqualified from sports participation; none of these individuals died during follow-up.
During 1976-1996, 49 athletes sustained sudden death. Soccer was the sport most commonly implicated, encompassing almost 50% of the deaths. As a result of successful screening, HC was responsible for only 2% of athlete sudden death, compared to 7.3% in the non-athlete population. Historical, physical, or EKG findings consistent with increased risk of cardiovascular disease were present at screening in 82% of athletes who died of arrhythmo- genic right ventricular cardiomyopathy (ARVC), the most common cause of sudden death among athletes in this study (22.4%) The authors conclude that there was a selective reduction in HC-induced sudden death among ath- letes, attributable to the screening evalu- ations. The authors also postulate that ARVC is suggested by the presence at screening EKG of PVCs with LBBB and inverted precordial T waves.
Corrado D, et al. N Engl J Med 1998; 339:364-369.
Orlistat for Weight Loss and Prevention of Weight Regain
Obesity is a major personal and public health problem throughout the world. After two decades of a relative pharmacotherapeutic vacuum, recently employed agents have been causally implicated in cardiovascular pathology. A new agent that would be efficacious without causing, in particular, serious cardiovascular sequelae would be very welcome.
Orlistat inhibits gastrointestinal lipases, hence reducing absorption of dietary fat. On a typical regimen of orli- stat 120 mg tid, a reduction of about 30% fat absorption could be anticipated. The current study enrolled men and women of BMI at least 28 for a double-blind, randomized, placebo-controlled parallel-group study (n = 688). In the first year of the study, patients were assigned to a hypocaloric diet (600 kcal/d deficit). In the second year, patients were placed on a eucaloric (weight maintenance) diet. Active treatment was 120 mg orlistat tid.
At the end of the first year, the active treatment group had lost about nine pounds more than the placebo group. In the second year, patients maintained on orlistat regained only half as much weight as placebo recipients. Surrogate end points such as total cholesterol, LDL, serum glucose, and insulin were more favorably affected by orlistat than placebo. Attesting to the overall tolera- bility of orlistat, in the first year of ther- apy, premature withdrawal was almost 30% more common in the placebo group. Gastrointestinal side effects were more common with active treat- ment. Orlistat may offer an attractive alternative for long-term palliation of obesity.
Sjostrom L, et al. Lancet 1998;352: 167-173.
Do ACE Inhibitors Protect Against Cancer Risk?
Much media attention has been drawn to the reports of alleged increased risk of cancer associated with use of some calcium channel blockers (CCB) in some hypertensive patient populations. ACE inhibitors are an increasingly popular antihypertensive therapeutic choice globally. There are several theoretic ways in which manipulation of the renin-angiotensin-aldosterone system might influence cancer growth. For instance, tumor growth requires neovascularization, which is known to be stimulated by angiotensin II (A-II). Some tumors have A-II recep- tors. Additionally, in blood vessel-free tissue culture, A-II enhances cell growth gene expression.
In this retrospective look, HTN patients seen at the Glasgow Blood Pressure Clinic (n = 5207) from 1980 through 1995 were compared based on use of ACE inhibitors, CCBs, diuretics, and beta blockers. The relative risks of both the incidence (RR = 0.72) and fatality rate for cancer (RR = 0.65) were substantially lower among persons receiving ACE inhibitors. This favorable difference began to be evident after three years therapy. The authors acknowledge that, although the observations attained in their analysis provide an engaging hypothesis, conclusive evidence will depend upon a specific randomized interventional trial.
Lever AF, et al. Lancet 1998;352: 179-184.
Clinical Scenario: The ECG shown in the figure was obtained from a 78-year-old man as part of his routine preoperative clearance evaluation. The patient had a history of ischemic heart disease and heart failure. He was on multiple medications. He was completely asymptomatic at the time this ECG was recorded. Would you clear him for surgery?
Interpretation: The rhythm is regular at a rate of between 55 and 60 beats/min. Notable for its absence is the lack of an upright P wave in lead II. Given that the QRS complex is narrow, this defines the rhythm as junctional. The small amplitude upright deflection in lead V1 may represent a retrograde P wave, albeit with a prolonged R-P interval. Otherwise, the axis is vertical, there is evidence of prior anterolateral infarction, and diffuse ST segment and T wave flattening is seen. However, there are no acute changes.
In view of the fact that the patient has underlying heart disease, one has to inquire if digoxin is among the multiple medications he is taking. In point of fact, this patient's serum digoxin level was in the toxic range.
Digoxin toxicity is notorious for producing a variety of cardiac arrhythmias, especially accelerated junctional rhythms. The presence of an underlying conduction disorder in this patient may have accounted for the relatively slow rate of this digitalis-induced arrhythmia. The patient's operation should be delayed until his digoxin level returns to the therapeutic range.