Clinical features of left main equivalent coronary disease.
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Biomedical subjects
Publications and source records attributed to J D Babb.
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A case of systemic lupus erythematosus (SLE) was complicated by ruptured chordae tendineae. The mechanisms responsible for severe cardiac dysfunction in SLE are discussed.
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A case is reported of aortic regurgitation resulting from a congenitally abnormal aortic valve. The left coronary cusp of the valve was small and adhered to the aortic wall, so that there was insufficient valve tissue to maintain diastolic valve competence. In addition, this rudimentary cusp completely occluded the left coronary ostium. The patient was treated successfully by valve replacement.
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.
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 less than 0.005). The total coronary score reflecting total extent of disease for diabetic patients was 371 (mean 10.0 +/- (SEM) compared to 594 for controls (mean 7.5 +/- 0.7, (P less than 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.
Current management of ventricular septal defect (VSD) after myocardial infarction (MI) is aimed at improving left ventricular (LV) performance by afterload reduction as a means of hemodynamic stabilization or shunt control. The current investigation was undertaken to determine whether primary manipulation of right venticular (RV) performance by afterload enhancement was an effective means of reducing MI-VSD shunting. In five open-chest dogs an external LV-RV shunt was created with pulmonary-systemic flow ratios (Qp/Qs) averaging 2.26:1. Inflation of a balloon-tipped catheter in the main pulmonary artery (PA) reduced average QP/Qs to 1.28:1 and shunt flow from 783 to 343 ml/min. However, this increase in RV afterload caused further significant increases in RV systolic and end-diastolic pressure and suggested that deterioration of RV function might be limiting the usefulness of this technique. To investigate whether inotropic support for the RV would overcome this limitation, a similar shunt was created in 11 open-chest swine. We then investigated the effects of dopamine, infused at 24, 60, and 120 mug/min, on QP/QS and other hemodynamic variables both with and without PA balloon inflation. Optimal shunt control was obtained when effects of dopamine were added to those of PA balloon inflation. Shunt flow that had been 1,633 ml/min was reduced to 892 ml/min with the PA balloon and reduced further to 757 ml/min with dopamine, which also lowered RV and LV end-diastolic pressure and reduced total systemic vascular resistance. In four other swine with left anterior descending ligations, PA balloon inflation and dopamine infusion again favorably affected hemodynamics. Epicardial mapping in these swine showed an increase in S-T segment displacement, suggesting that the cumulative effect of these interventions allowed hemodynamic improvement at the expense of enhanced ischemic injury. These data indicate that acute RV outflow obstruction with a balloon catheter is an effective means of temporarily reducing acute ventricular shunting and that dopamine may be a useful pharmacological agent to use with RV afterload manipulation to stabilize a patient prior to transfer to a medical center for more definitive therapy.
Several reports in the literature and our experience prior to 1974 support the thesis that operative risk in patients with acquired heart disease and poor ventricular function (as assessed by a biplane ejection fraction [EF] less than or equal to 0.40) was very significantly increased over the risk in patients with normal ventricular function. These results led to disagreement in the literature regarding the advisability of surgery in patients with poor ventricular function. Various EFs from less than 0.31 to less than 0.50 were suggested as contradicting elective surgery, while more aggressive groups recommended surgery in all patients with angina. Precise comparison of the results reported by different groups was not always possible because of the common reliance on single-plane right anterior oblique ventriculograms, which tend to underestimate EF and overestimate operative risk. Using biplane ventribulograms for accurate estimation of EF, we have demonstrated a significant reduction in 30-day operative risk to a clinically acceptable 3 percent (1/32) for single valve replacement and aortocoronary surgery patients with poor ventricular function (EF less than or equal to 0.40) during 1974. Considering the high risk of medically treated patients with reduced ventricular function, these results support further evaluation of surgical palliation for patients with valvular or coronary heart disease and reduced ventricular function.
Coronary arteriovenous fistula is an uncommon, although not rare, congenital cardiac malformation, especially in the adult. Most such reported such cases have involved but a single coronary vessel. This report documents the second case of coronary arteriovenous fistulae involving the right and circumflex coronary vessels draining into the coronary sinus. At the present time the patient is free of definite ischemic symptoms or obvious impairment of hemodynamic function and is being followed-up medically.
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.
Left ventricular (LV) myocardial function and the influence on LV pump performance of associated coronary arterial disease, of outflow obstruction and its consequences, and of altered ventricular pressure-volume characteristics were examined in a representative group of 28 adult patients with symptomatic severe aortic stenosis (valvular orifice area less than 0.50 sq cm/sq m). Eighteen patients (64%) exhibited depressed LV pump performance with levels of ejection fraction less than 0.50. In seven patients, coronary arterial disease documented by either arteriographic studies or postmortem analyses was associated with a segmental (i.e., nonhomogeneous) LV contractile disorder consistent with previous myocardial infarction. In the remaining 11 patients a homogeneous LV contractile disorder was the result of chronic outflow obstruction and its consequences. The possibility that reduced ventricular performance might be accounted for by increased afterload could not be supported by significant correlation between LV contractile characteristics (estimated from the ejection fraction and the mean circumferential fiber shortening rate) and indices of afterload (including LV systolic pressure, aortic valvular orifice area, and mean systolic wall tension). This observation suggested that myocardial hypertrophy and other consequences of longstanding obstruction to outflow played a primary role in depression of LV performance in these patients. Left ventricular end-diastolic volume was abnormal in all but three patients with depressed LV function; this increase was accompanied by a disproportionately greater increment in end-diastolic pressure, suggesting that reduced distensibility limited the ability of the ventricle to compensate for reduced contractile performance by means of the Starling mechanism.
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In order to evaluate the duration of the biologic effects of propranolol after the drug was discontinued, we evaluated a variety of noninvasively determined hemodynamic parameters. Significant depression was found in the heart rate (18 per cent), cardiac output (13 per cent) (determined echocardiographically), and the triple product of blood pressure, heart rate, and systolic ejection time (16 per per cent) during administration or propranolol (200 mg. per day) to 9 normal volunteers. Significant depression of these parameters was present 12 hours after discontinuing the drug. By 12 hours, serum propranolol levels had returned 90 per cent toward their base line; however, at the same time, the heart rate and cardiac output had returned only 19.4 and 14.3 per cent toward their base-line values, and the triple product had returned 41 per cent toward its baseline. By 36 hours no biologic effect was seen. Thus if propranolol were discontinued 2 days prior to cardiac surgery, no significant biologic effect would remain to complicate the patient's postoperative course.