Lawrence J. Laslett

The Worldwide Environment of Cardiovascular Disease: Prevalence, Diagnosis, Therapy, and Policy Issues: A Report From the American College of Cardiology

The environment in which the field of cardiology finds itself has been rapidly changing. This supplement, an expansion of a report created for the Board of Trustees, is intended to provide a timely snapshot of the socio-economic, political, and scientific aspects of this environment as it applies to practice both in the United States and internationally. This publication should assist healthcare professionals looking for the most recent statistics on cardiovascular disease and the risk factors that contribute to it, drug and device trends affecting the industry, and how the practice of cardiology is changing in the United States.

Evidence of Myocardial Injury During Prolonged Strenuous Exercise

These preliminary data suggest that extremely prolonged intense exercise may induce subclinical myocardial injury. Although questions of assay interference exist, the importance of this finding has prompted planning of a larger study using a methodologically more specific assay.

Symptomatic and silent myocardial ischemia during exercise testing in coronary artery disease

During exercise by patients with coronary artery disease (CAD), electrocardiographic evidence of myocardial ischemia may precede the onset of angina or may be unassociated with angina, even at peak levels of stress. However, neither the precise incidence of silent versus symptomatic ischemic episodes nor their interrelation in this setting has been clearly defined. The prevalence of silent and symptomatic myocardial ischemia during treadmill exercise testing was determined in 92 patients with angiographically documented CAD. The study group comprised 77 men (84%) and 15 women (16%) of mean age 57 years (range 32 to 79). Exercise testing resulted in ischemic ST-segment depression (greater than or equal to 1 mm for greater than or equal to 80 ms) only or in association with delayed (greater than or equal to 1 minute) angina in 39 patients (42%); angina only or in association with delayed ST-segment depression occurred in 42 patients (46%); and simultaneous occurrence of angina and ST-segment depression was noted in 11 patients (12%). Analysis of clinical, exercise and angiographic factors (age, sex, history of myocardial infarction, heart rate, maximal ST-segment depression, extent of CAD and left ventricular ejection fraction) revealed no significant correlation with the frequency of symptomatic and silent myocardial ischemia during exercise. Asymptomatic myocardial ischemia occurred commonly during exercise in patients with CAD, but there were no differences in the characteristics of patients with symptomatic and asymptomatic episodes.

Increase in myocardial oxygen consumption indexes by exercise training at onset of ischemia in patients with coronary artery disease.

It has been unclear whether exercise training of patients with coronary artery disease increases the level of myocardial oxygen consumption, as indicated by heart rate and double product of heart rate and systolic blood pressure, at which electrocardiographic evidence of myocardial ischemia develops. To assess this question we evaluated the experience of 10 patients with coronary artery disease who underwent a modest-level exercise training program for 6 months. All of these subjects had achieved a training effect, had developed electrocardiographic evidence of ischemia during initial exercise testing, had not increased the amount of cardiac medication taken, and had not been taking digoxin. After completion of the training period, the mean heart rate at which electrocardiographic evidence of ischemia developed increased from 107 +/- 19 to 119 +/- 23 beats/min (p less than .05) and the mean double product increased from 166 +/- 18 to 209 +/- 51 X 10(2) mm Hg X beats/min (p less than .05). Eight of the 10 patients demonstrated an increase in heart rate at onset of ischemia (p less than .02), and seven of the eight in whom double product could be assessed manifested an increase in this parameter at onset of ischemia (p less than .05). Thus the rate of myocardial oxygen consumption at which myocardial ischemia develops, as indirectly assessed by heart rate and double product, can be favorably altered by 6 months of moderate-level exercise training.

Selenium supplementation does not improve vascular responsiveness in healthy North American men.

Selenium is an essential trace nutrient required for the synthesis of selenoproteins such as glutathione peroxidase and thioredoxin reductase, the major forms of selenium in the endothelium that have important functions relevant to inflammation and cardiovascular disease. Selenium deficiency is associated with cardiomyopathy and sudden cardiac death in animals, and a low selenium status is associated with cardiovascular disease in humans. Endothelial dysfunction, measured as the impaired flow-mediated vasorelaxation of the brachial artery, is a reliable indicator of future cardiovascular disease risk in healthy individuals. To test whether selenium supplementation affects endothelial function, we conducted a randomized, placebo-controlled trial in healthy men who were administered 300 microg of selenium a day as high-selenium yeast for 48 wk. Brachial artery responsiveness to transient occlusion was assessed at baseline and after 24 and 48 wk of supplementation. The supplementation increased the selenium concentration by more than half in blood plasma and erythrocytes. However, there was no effect of selenium on arterial diameter or blood flow rate before or after transient occlusion or on the maximum dilated diameter after the administration of nitroglycerin. This study indicates that selenium supplementation is not likely to improve endothelial function or peripheral arterial responsiveness in healthy North American men receiving adequate selenium from their diets.

Lack of Detection of Myocardial Injury During Competitive Races of 100 Miles Lasting 18 to 30 Hours

Competitors in an ultramarathon performed under extreme conditions did not demonstrate evidence of subclinical myocardial injury, as determined using cardiac troponin T as a marker. This finding refutes previous data and is likely due to utilization of an improved assay for cardiac troponin T that minimizes cross reactivity with skeletal muscle troponin T.

Efficacy of exercise training in patients with coronary artery disease who are taking propranolol.

The effects of beta-adrenergic blockade on the efficacy of exercise training in patients with coronary artery disease were assessed in a community-based cardiac rehabilitation program. Twenty-five patients took no beta-adrenergic-blocking agent and 17 patients took a constant dose of propranolol during the 3 month study period. Individual exercise prescriptions consisted of an intensity of 70% of maximal workload monitored by heart rate, performed 20 min each session, three sessions per week. Both groups improved in maximal exercise capacity: from 8.7 +/- 1.9 (mean +/- SD) to 9.7 +/- 2.1 mets (p less than .01) in those not taking propranolol and from 6.6 +/- 1.5 to 7.7 +/- 1.8 mets (p less than .01) in those taking the drug. At a workload of 70% of maximal achieved at pretraining testing, heart rate decreased with training from 123 +/- 19 to 113 +/- 17 beats/min (p less than .01) in those not taking propranolol and from 97 +/- 14 to 92 +/- 12 beats/min (p less than .05) in those taking the drug. At a workload of 85% of pretraining maximum, heart rate similarly was lowered with training from 138 +/- 17 to 126 +/- 17 beats/min (p less than .01) in those not taking a beta-blocker and from 107 +/- 13 to 102 +/- 13 beats/min (p less than .02) in those taking propranolol. Thus patients with coronary disease who take propranolol have the same potential to benefit from physical training as patients who do not take beta-blockers, and exercise does not need to be modified because of the drug.

Unique spontaneous coronary artery dissection in an elderly woman.

Spontaneous coronary artery dissection is a rare condition, typically occurring in younger women. A 75-year-old woman with this condition, 17 years older than previously reported, is described, including her unusual presentation with angina rather than infarct. The 112 previously reported cases are summarized and treatment options discussed.

Sublingual Nitroglycerin Administered by Spray versus Tablet: Comparative Timing of Hemodynamic Effects

The comparative timing of hemodynamic alterations by sublingual nitroglycerin administered by spray vs. tablet has not been studied. Similarly, the directly measured comparative effects on left ventricular pressures have not been reported. To investigate these issues, we analyzed 49 patients undergoing elective diagnostic cardiac catheterization who were randomized to receive 0.4 mg sublingual nitroglycerin by either spray or tablet. Before administration of contrast medium, control determinations of left ventricular end-diastolic and systolic pressures and heart rate were done. These parameters were then evaluated at half-minute intervals for 5 min. Left ventricular end-diastolic pressure was reduced similarly in both groups, with the reduction achieving significance at 1.5 min in the spray and 2.0 min in the tablet group. Lowering of the left ventricular systolic pressure was also similar in the two groups, reaching significance at 2.5 min with spray and 2.0 min with tablet. Heart rate increased significantly by 2.0 min in the tablet group but did not change in the spray group. These findings were not altered by the level of resting left ventricular end-diastolic pressure or use of chronic nitrates. Thus, we found nitroglycerin to be similarly effective in timing and extent of response whether administered by spray or tablet, though the difference in heart rate responses remains unexplained.

Acute myocardial infarction in hemoglobin SC disease.

Although there are reports of myocardial infarction (MI) in patients with sickle cell diseases, an antemortem diagnosis of acute MI in a patient with compound heterozygous hemoglobin SC disease has not been reported. Herein, we present a patient with hemoglobin SC who suffered an acute MI. She had typical chest pain for myocardial ischemia, associated with ST elevations on the electrocardiogram (EKG) and elevations of cardiac injury markers diagnostic of infarction. The patient was treated with conventional therapies for acute coronary syndrome and also emergent red blood cell exchange. Interestingly, coronary angiography was completely normal in this patient. Potential mechanisms and management for acute MI in patients with sickle cell disease are discussed.