David M. Leaman

Diffuse coronary artery disease in diabetic patients: fact or fiction?

To compare angiographically-determined coronary artery disease in diabetic patients with controls, 1,653 patients coming to cardiac catheterization were reviewed retrospectively to find 37 diabetic and 79 control patients matched for sex, age (± 3 years), and risk factors (hypertension, hyperlipidemia, and smoking). The severity of coronary artery disease was assessed using an angiographic grading system. The following results were obtained: 16 of 37 diabetic patients (43%) had three-vessel disease compared to 20 of 79 controls (25%). Seventy-six of 111 (68%) diabetic vessels were diseased compared to 110 of 237 control vessels (46%) (P < 0.005). The total coronary score reflecting total extent of disease for diabetic patients was 371 (mean 10.0 ± 1.0 (SEM)) compared to 594 for controls (mean 7.5 ± 0.7, P < 0.01). Diabetic patients had a statistically similar number of diffusely diseased vessels as controls (28% vs 22%). There were only three of 76 diabetic vessels (4%) considered inoperable compared to seven of 110 (6%) control vessels. We conclude that diabetic patients with chest pain have more coronary artery disease than nondiabetics, but no more diffuse or inoperable disease.

Enhanced metabolic vasodilation secondary to diuretic therapy in decompensated congestive heart failure secondary to coronary artery disease

Since sodium and water retention have been implicated as major factors limiting maximal metabolic vasodilation in congestive heart failure (CHF), the effect of rigorous diuresis on maximal vasodilatory capacity was studied systematically in 9 subjects hospitalized with decompensated CHF. Peak reactive hyperemic blood flow, measured by strain-gauge plethysmography, was used as an index of maximal vasodilatory capacity. After 24 hours of diuresis and a 2.2-kg weight loss, maximal flow increased from 19.9 to 26.1 ml/min X 100 ml (p less than 0.05). Despite a further 1.4-kg weight loss between 24 and 48 hours, maximal blood flow increased no more (26.1 to 25.8 ml/min X 100 ml). Since blood pressure did not change significantly, minimal forearm resistance and maximal conductance showed similar improvements. It is unlikely that vasoconstrictor hormone changes could account for this effect since a marked decrease in plasma norepinephrine occurred in only 2 of 8 subjects and plasma renin activity decreased in only 1 subject. As a group there was no significant change in norepinephrine level, which remained substantially above normal (1,525 to 1,148 pg/ml), or in plasma renin activity (12.3 to 18.9 ng/ml/hour). Because the improvement in vasodilator capacity reached a plateau by 24 hours despite continued diuresis, and because peak reactive hyperemic blood flow was still 32% below normal, it is suggested that a second mechanism besides sodium and water retention is responsible for a significant portion of the impaired peripheral vasodilation in CHF.

Geometry of Left Ventricular Contraction in the Systolic Click Syndrome Characterization of a Segmental Myocardial Abnormality

Left ventricular (LV) shape change during systole was characterized in nine patients with typical clinical findings of the systolic click syndrome (SCS) by means of cineangiographic measurements of three segmental diameters of the LV cavity and of the mitral valve ring (MVR) and contrasted with findings in eight patients with normal LV function. In the latter group, shortening of the proximal, midventricular, and apical segment diameters was comparable, averaging 38.6, 40.3, and 46.8%, respectively; MVR shortening averaged 31.8%. The velocity of fiber shortening, estimated as mean circumferential fiber shortening rate (mean FSR), was also similar in the three segments (1.66, 1.84, and 2.09 circ/sec). In patients with SCS, the extent of shortening and mean FSR in the proximal ventricular segment were consistently reduced (average 22.2%, P < 0.005; and 0.96 circ/sec, P < 0.025 respectively), and the MVR exhibited either reduced extent of contraction (four patients) or was unchanged or increased in diameter during systole (five patients). However, shortening of the midventricular and apical segments was normal, averaging 37.5 and 40.5%, respectively, as was the mean FSR in these segments (averages 1.60 and 1.70 circ/sec).These findings are consistent with a primary disorder of the myocardium in SCS localized to the inflow region of the left ventricle.

Recurrent Pulmonary Emboli Secondary to Right Atrial Thrombus Around a Permanent Pacing Catheter: A Case Report and Review of the Literature

A case report and review of the literature.

Propranolol rebound—A retrospective study

To assess the effects of sudden withdrawal of propranolol on inpatients with coronary artery disease, 102 patients admitted for cardiac catheterization were evaluated. Criteria for inclusion in the study were angiographically documented coronary artery disease, propranolol therapy at a mean daily dose of at least 80 mg and abrupt discontinuation of propranolol therapy before catheterization. There were 55 patients (mean age 52.5) who discontinued propranolol therapy (mean daily dose 127 mg) and a control group of 47 patients (mean age 53) who continued to receive propranolol (mean daily dose 143 mg). The criteria for morbidity were death, myocardial infarction or change in pain pattern. In the withdrawal group there were no deaths, one myocardial infarction judged to be related to catheterization and only one instance of a change in pain pattern. Thus, propranolol rebound appears to occur infrequently among hospitalized patients with reduced activity.

Effects of morphine sulfate on human coronary blood flow.

Because morphine causes coronary vasoconstriction in conscious dogs, human coronary blood flow was measured with the thermodilution technique before and after administration of morphine sulfate, 0.2 mg/kg body weight (maximum 15 mg) intravenously, in 10 patients to determine if the canine experience is clinically applicable. Coronary blood flow increased from a baseline value of 104.4 +/- 13.4 (mean +/- standard error of the mean) to 113.0 +/- 17.4 ml/min (difference not significant) 15 minutes after the administration of morphine. Baseline coronary vascular resistance was 1.14 +/- 0.19 mm Hg/ml/min; 15 minutes after morphine administration the resistance value was 1.02 +/- 0.17 (P less than 0.025). There was no significant change between baseline values and values 15 minutes after morphine administration in systemic mean arterial pressure (98.2 +/- 5.3 to 92.8 +/- 4.7 mm Hg); heart rate (69.5 +/- 3.5 to 72.6 +/- 3.4 beats/min), left ventricular ejection time (0.345 +/- 0.009 to 0.342 +/- 0.007 second) or tension-time index (2,324 +/- 128 to 2,291 +/- 149 mm Hg/sec per min). The slight coronary vasodilation noted after morphine administration in this study is in marked contrast to the significant coronary vasoconstriction demonstrated in the unanesthetized dog.

Safety of short-term percutaneous arterial cannulation.

The technique of percutaneous arterial cannulation has been used frequently in critical patients undergoing long-term hemodynamic evaluation. When arterial cannulae have been left in place for one or more days, they have been reported to be associated with considerable morbidity, including arterial thrombosis.’*2 Because of the reported complications, institutional committees reviewing human studies have questioned the risk/benefit ratio in studies employing the direct recording of blood pressure. However, no substantial morbidity data are available when an arterial cannula has been left in place for studies of short duration, less than 4 hours. Therefore, this prospective study was undertaken to evaluate the safety of arterial cannulation used on a short-term basis for the continuous monitoring of systemic arterial pressure during routine diagnostic cardiac catheterization.

Angina pectoris: Diagnosis and treatment

The physician who understands the pathophysiology of angina pectoris can apply rational therapeutic measures based on an appreciation of the determinants of myocardial oxygen supply and demand. Most patients with angina secondary to coronary atherosclerosis can be treated conservatively using a systematic approach that includes correction or removal of underlying causes or precipitating factors and the judicious use of sublingual nitroglycerin. In patients with more resistant angina, use of oral or topical nitroglycerin or sublingual isosorbide dinitrite as well as propranolol can be advised. Aortocoronary bypass surgery can offer significant improvement in carefully selected patients with frequent angina poorly controlled by medical therapy. The most important consideration in the treatment of angina is protection of coronary blood flow reserve by primary prevention of the atherosclerotic process itself. All individuals from families prone to coronary artery disease should be evaluated for alterable risk factors, the most important being cigarette smoking, hypertension, and hypercholesterolemia. Considering the high risk of unheralded sudden death in previously asymptomatic patients with coronary atherosclerosis, angina can, in a sense, be considered a fortunate harbinger of coronary stenosis, identifying candidates for secondary preventive measures aimed at retarding the progression of vascular disease. More importantly, angina serves as an index for detecting families at high risk of coronary artery disease, in whom early application of primary prevention may afford a more promising outlook.

Diagnosis and Management of Myocardial Ischemia in the Postoperative Period

The determinants of myocardial oxygen consumption, the consequences of coronary artery atherosclerosis, angina, and myocardial infarction, and their therapy are considered in this article. The mechanism of action of the drugs used in the therapy of myocardial ischemia and the rationale for their use is discussed. A plan of in-hospital rehabilitation for the postoperative myocardial infarction patient is also offered.