[The effect of nitrous oxide on experimentally induced spasm of the coronary vessels].
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Coronary effects of Ca -channel blockers mibefradil and amlodipine were compared in conscious dogs. Ten dogs were instrumented for measurement of aortic and left ventricular pressures, circumflex coronary blood flow velocity (CBFv), and coronary diameter (CD). A permanent catheter was implanted in the circumflex coronary artery. At doses having no systemic effects (7.5-150 micro g/kg), mibefradil and amlodipine increased CBFv and CD dose dependently. At the same dose, mibefradil increased less CBFv than amlodipine. However, for a similar increase in CBFv induced by amlodipine, mibefradil increased CD more. BAY K8644, an L-type Ca -channel agonist, prevented the CBFv and CD responses to amlodipine, but minimally affected the coronary responses to mibefradil. Intracoronary isoproterenol (6 ng/kg) increased LV dP/dt max, CBFv, and CD. Amlodipine markedly altered these responses, while mibefradil did not affect LV inotropic response and slightly altered CBFv response to isoproterenol. Thus, in conscious dogs, both mibefradil and amlodipine exert coronary vasodilation, with different patterns on coronary conductance and resistance vessels and during beta-adrenergic stimulation. These differences could be related to their actions on different Ca channels.
Coronary perforation can be managed with prolonged balloon inflations, covered stents, or embolization of the vessel. We report on a case of a balloon-induced perforation of the distal left anterior descending artery, that was sealed by injecting preclotted autologous blood through the balloon catheter lumen at the site of the perforation. The patency of the distal vessel was maintained.
Ventricular septal defect following acute myocardial infarction is a rare but life-threatening complication. Early surgical closure improves survival but carries a considerable risk. Percutaneous transcatheter closure is an alternative but experience to date is limited. We report a case of successful transcatheter closure of postmyocardial infarction ventricular septal defect (VSD) in a 55-year-old male with the Amplatzer muscular VSD occluder device and complete percutaneous revascularization with successful multivessel coronary stenting for three-vessel disease as a staged procedure. The technique and its potential use as an alternative to surgical approach for treatment of acute myocardial infarction and its complication (VSD) are discussed.
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A 44-year-old German fell ill in Libya, where he had been living for 10 years, with high fever, rigor and a nonitching centrifugally spreading macular rash, which had spared the head, hands and soles. In addition, a systolic cardiac murmur was heard. The Weil-Felix reaction had a titre rising within 3 days from 1:160 to 1:640, confirming the diagnosis of rickettsial disease, the total clinical picture indicating typhus. On treatment with chloramphenicol (1 g three times daily i.v.) the fever subsided within 5 days. On the ninth day treatment was changed to oral doxycyclin, 200 mg daily for 3 weeks. Echocardiography surprisingly revealed a floating thrombus, about 4 x 8 cm, attached to the hypo- and even akinetic apex of the left ventricle. In addition there was single-vessel coronary disease. Since the segmental contraction abnormality persisted after the typhus had been cured, a causal connection with the rickettsial disease is unlikely. The thrombus was removed at the time of a aortocoronary bypass operation: his course has been unremarkable since then.
UNLABELLED: Regional myocardial blood flow was studied at rest in 72 patients with a typical history of angina pectoris and/or myocardial infarction using the 133Xenon clearance technique. 62 patients had isolated greater than 50% obstructions of the left anterior descending or of the left circumflex branch, 10 patients had segmental asynergy yet no or only minimal (less than 35%) coronary obstructions. In each patient, flow of the poststenotic (asynergic) LV wall area was related to flow of the normal area (= 100%). Coronary obstructions were measured in multiple projections using a vernier, and segmental wall motion was quantitated by systolic halfaxial shortening. RESULTS: A progressive decrease of poststenotic flow was found with increasing severity of coronary obstructions: in relation to the respective normal areas, poststenotic flow was reduced to 84% distal to 50-75% obstructions (p less than 0.01), to 75% distal to 76-90% obstructions (p less than 0.0005), and to 67% distal to less than 90% obstructions (p less than 0.0005). However, analysis of poststenotic LV wall motion suggested that flow was correlated more closely to poststenotic wall motion: in hypokinetic areas, flow was reduced to 75% (p less than 0.0005), and in akinetic areas to 55% (p less than 0.0005) whereas in poststenotic areas with normal wall motion resting flow was normal regardless of the severity of coronary obstructions. Furthermore, the reduction of flow in asynergic areas of patients without coronary obstructions was comparable to flow in asynergic areas supplied by severely stenosed vessels. Thus in chronic coronary heart disease, regional myocardial blood flow correlates not only to the severity of coronary obstructions but also to segmental left ventricular wall motion.
UNLABELLED: Cigarette smoking is a major risk of coronary artery disease. Acetylcholine-induced coronary artery constriction has been reported in patients with normal coronary arteries and other risk factors. To evaluate coronary artery endothelial function in smokers, coronary artery responses to acetylcholine (10(-8) M to 10(-5) M) were analyzed by quantitative angiography in 5 young heavy-smokers and in 5 age-matched nonsmokers. All patients were normotensive, had normal left ventricular function and coronary arteries. Cholesterol, triglycerides, high- and low-density lipoproteins were within normal range. Vessel dimensions were measured on 4 segments of left coronary artery in all patients. In smokers, no change was produced at 10(-8) M and 10(-7) M acetylcholine concentration, but progressive diameter reduction was observed at 10(-6) M and 10(-5) M acetylcholine concentration. In nonsmokers, a dose-dependent dilation was produced from 10(-8) M to 10(-6) M acetylcholine concentration. No change was observed at 10(-5) M acetylcholine concentration. In the 2 groups, all segments dilated similarly after intracoronary isosorbide dinitrate. CONCLUSION: This study reveals that in heavy-smokers the response of normal coronary arteries to acetylcholine is altered. Thus, endothelial dysfunction may be an early marker for coronary events in cigarette smokers.
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The severity of the regional wall motion and its effects on the global left ventricular diastolic filling were analyzed with use of radionuclide techniques in 19 patients with isolated disease of the left anterior descending coronary artery with previous myocardial infarction. Regional maximum inward movements in the noninfarcted lateral region occurred at a time close to the global end-systole, but occurred far beyond the global end-systole in the infarcted septal and apical regions, resulting in the occurrence of the regional asynchronous wall motion between the infarcted and noninfarcted regions after the global end-systole. A positive correlation between this end-systolic asynchronous wall motion and the asynchronous filling in early diastole was found (r = 0.69, p less than 0.001). A negative correlation between the asynchronous filling in early diastole and the global peak filling rate was also found (r = -0.58, p less than 0.01). Thus, the end-systolic regional asynchronous wall motion causes the subsequent regional asynchronous filling in early diastole, which may cause impairment of the global left ventricular filling in patients with single-vessel coronary artery disease with previous myocardial infarction.
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Anomalous origin of the left main coronary artery from the right anterior aortic sinus is a rare condition (0.02 to 0.07%) and its clinical significance is sometimes controversial. The authors present the case of a 44-year-old female with this anomaly and septal course with clinical, electrocardiographic, scintigraphic and cineangiographic evidences of myocardial infarction without coronary lesions. Literature is reviewed regarding diagnosis, clinical significance, pathophysiology and management. It is probably the first evidence of the potential danger of this anomaly with septal course.
Anomalous origin of the left coronary artery from the pulmonary artery is a rare congenital abnormality with a poor prognosis in the newborn. Adult forms are, therefore, very rare, presenting with angina, cardiac failure or sudden death. The authors report the case of a 41 year old woman who was asymptomatic until admitted as an emergency after ventricular fibrillation. Coronary angiography established the diagnosis. Despite the absence of reversible ischaemia on exercise myocardial scintigraphy, the patient underwent coronary bypass surgery of the left anterior descending artery with a pediculated internal mammary artery graft and closure of the left coronary ostium on the pulmonary artery. The echocardiographic abnormalities regressed within a few weeks. An automatic defibrillator was not implanted. The physiopathology of this rare cardiac lesion, the mechanisms of sudden death and the different techniques of surgical repair are discussed.