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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., (Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

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.

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.

Background: Ischemic preconditioning is characterized by the limitation of infarct size or ischemic signs after one or more brief episodes of ischemia, a process that probably involves stimulation of adenosine receptors. One human model of ischemic preconditioning is repetitive occlusion of a coronary artery during angioplasty. By using this method of inducing ischemia, we tested the hypothesis that blockade of adenosine receptors with aminophylline would abolish ischemic preconditioning in human beings., Methods: Twenty-six patients undergoing angioplasty were randomly assigned to receive either aminophylline (6 mg/kg IV) or placebo before repetitive coronary occlusion (two 2-minute occlusions separated by 5 minutes). ST-segment changes on the surface electrocardiogram were used as a measure of myocardial ischemia. Serum theophylline levels and the conduction response to an intravenous bolus of adenosine were used to assess the efficacy of adenosine receptor blockade., Results: Repetitive coronary occlusion resulted in a reduction in ST-segment shift in 9 of 13 patients given placebo. In contrast, 9 of 13 patients receiving aminophylline had an increase in ST-segment shift on the second occlusion (P =.002). Patients receiving aminophylline (mean serum theophylline level of 8.38 +/- 0.45 mg/dL) did not have significant conduction block with intravenous adenosine., Conclusions: Repetitive coronary occlusion reduces the signs of ischemia in human beings, a process limited by blockade of adenosine receptors.

A 29-year-old woman with active systemic lupus erythematosus (SLE) sustained an anterior myocardial infarction and demonstrated angiographic evidence of multiple, diffuse coronary aneurysms. Coronary artery aneurysms have been reported in 11 prior cases of patients with SLE. A Medline search of the literature revealed no prior reports of extensive aneurysmal dilatations involving all three main coronary arteries (left anterior descending, left circumflex, and right coronary arteries).

Background: Endogenous production of bradykinin (BK) has been postulated to cause hemodynamic changes and cardiac pain during myocardial ischemia, presumably because of the stimulation of cardiac afferent fibers., Methods: To test the hypothesis that BK results in cardiac reflex responses and can cause the sensation of angina, 10 patients with and without coronary atherosclerosis had BK injected into their right (RCA) and left (LCA) coronary arteries in graded concentrations up to 10(-5) m. Patients were monitored for hemodynamic changes and the presence and quality of pain., Results: Intracoronary BK 10(-5) m caused a significant reduction in blood pressure in most patients with either injection into the RCA or LCA (RCA: 151 +/- 10/90 +/- 5 mm Hg to 119 +/- 11/70 +/- 6 mm Hg, LCA: 161 +/- 11/88 +/- 6 mm Hg to 118 +/- 10/65 +/- 6 mm Hg) that began 12 to 14 seconds after injection. Injection into the LCA also resulted in a significant increase in heart rate (69 +/- 4 to 81 +/- 7 beats/minute), while injection into the RCA did not. Pain occurred after changes in blood pressure in all but one patient, which was present in 5 of 9 patients with RCA injection and 8 of 9 patients with LCA injection, and was often associated with flushing and nausea. Pain caused by BK was not similar to previous clinical ischemic pain in the patients with coronary atherosclerosis., Conclusions: The absence of a chronotropic response associated with arterial hypotension following injection of BK into the RCA is consistent with activation of cardiac vagal afferents in the left ventricle. The latency and quality of pain in these patients following injection of BK suggests that, while BK is nociceptive, it likely is not the cause of angina in patients with myocardial ischemia.

Conventionally, if an exercise electrocardiogram does not show evidence of ischemia, the patient must have achieved at least 85% of the predicted maximum heart rate for that test to be considered negative. However, no documentation of the validity of this practice exists. Thus, we evaluated the exercise electrocardiograms of 164 patients who had also undergone coronary angiography within 6 months of the exercise test. The predictive value of a negative exercise electrocardiogram was determined for each percentage point between 50 and 90% of the age-predicted maximum heart rate achieved or exceeded. The predictive value was found to increase modestly between 65 and 80% of the predicted maximum heart rate with no major changes above or below this range. Thus, it appears reasonable (in the setting of a hospital-based exercise laboratory) to either consider a negative exercise electrocardiogram as a valid finding if at least 80% of the predicted maximum heart rate is achieved, or preferably to simply report the negative finding with the percent maximum heart rate attained and the proviso that the predictive value of the test is progressively improved as higher heart rates are attained.

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.

Although cardiac catheterization-related infections are rare, caps and masks are often worn to minimize this complication. However, documentation of the value of caps and masks for this purpose is lacking. We, therefore, prospectively evaluated the experience of 504 patients undergoing percutaneous left heart catheterization, seeking evidence of a relationship between whether caps and/or masks were worn by the operators and the incidence of infection. No infections were found in any patient, regardless of whether a cap or mask was used. Thus, we found no evidence that caps or masks need to be worn during percutaneous cardiac catheterization.

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.

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.

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.

Severe tachycardia, ventricular ectopy, and sodium retention manifested by hemodynamic deterioration developed with hydralazine hydrochloride therapy in chronic coronary heart disease with congestive failure refractory to digitalis, diuretics, and nitrates. Coronary care unit admission with Swan-Ganz catheterization corrected hemodynamics by sodium nitroprusside treatment after hydralazine withdrawal. Satisfactory cardiac performance with oral long-acting nitrates were unsuccessful. However, the new oral vasocilator, prazosin hydrochloride, achieved considerable hemodynamic benefit by greatly reducing elevated left ventricular filling pressure and increasing severely depressed cardiac index to normal, accompanied by striking symptomatic improvement. Furthermore, long-term enhancement of cardiac dynamics and salutary functional status was maintained by ambulatory oral prazosin therapy for several months. This experience demonstrates the favorable alternative of prazosin nitroprusside-like actions over hydralazine-nitrate therapy in heart failure therapy and emphasizes prazosin's utility when untoward side effects to hydralazine develop.

The "positive" stress ECG in an asymptomatic individual should be interpreted cautiously, using both the details of the test results and details of the clinical history. The central concept that this test, in conjunction with the patient's clinical situation, does not yield an absolute answer regarding the presence of coronary artery disease, but rather a likelihood of the presence or absence of disease, forms the basis of this interpretation and the framework in which to make decisions regarding the advisability of further testing. In general, those asymptomatic individuals with a low posttest probability of disease should be followed clinically, those with an intermediate likelihood or strong personal concern should undergo further noninvasive testing, and only in those few with a high likelihood of disease after stress ECG testing should immediate coronary angiography be considered.

The second-order nonlinear differential equation for the rotation of Mercury implies locked-in motion when the period is within the range where e is the eccentricity and T is the period of Mercury's orbit, the time t is measured from perihelion, and lambda is a measure of the planet's disiortion. For values near 2T/3, the instantaneous period oscillates about 2T/3 with period (21lambdae/2)T.