Coronary artery stenosis complicating coronary angioplasty: report of six cases.
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Biomedical subjects
Publications and source records attributed to S J Gulotta.
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The resting and exercise hemodynamics in seven patients with pericardial constriction and in one patient with cardiac amyloidosis are described. Equalization of left and right heart diastolic filling pressures was observed in all cases, both at rest and during exercise. This hemodynamic response, although typical, should not be considered pathognomonic of pericardial constriction.
The evaluation of angina pectoris in patients with idiopathic hypertrophic subaortic stenosis is difficult in those in the age group prone to coronary artery disease. Ten patients with angina pectoris, normal coronary angiograms and idiopathic hypertrophic subaortic stenosis were studied with thallium-201 myocardial imaging performed in conjunction with submaximal treadmill exercise testing. The resting electrocardiogram demonstrated left ventricular hypertrophy with S-T segment abnormalities in seven patients, thereby vitiating the further increase in S-T segment abnormalities that developed in these patients during exercise or in the postexercise period. Of the three patients with a normal resting electrocardiogram, one had significant exercise-induced S-T segment depression. Thallium-201 myocardial imaging revealed no significant perfusion defects in 9 of the 10 patients (90 percent). In one patient with severe left ventricular hypertrophy significant perfusion defects developed after exercise that were not present at rest. Stress thallium-201 myocardial perfusion imaging is a useful noninvasive technique that assists in ruling out the presence of significant coronary artery disease in patients with idiopathic hypertrophic subaortic stenosis.
Four members of a family presenting with sinus bradycardia, a short P-R interval, intraventricular conduction defects, recurrent supraventricular tachycardia (SVT), syncope, and cardiomegaly had His bundle studies and were found to have markedly shortened A-H intervals (30 to 55 msec.) with normal H-V times (35 to 50 msec.). Right atrial pacing at rates as high as 170 to 215 per minute failed to increase the A-H or H-V intervals significantly. The data are compatible with the presence of an A-V nodal bypass tract (James bundle) or even complete absence of an A-V node. Ventricular pacing and spontaneous ventricular premature beats resulted in a short ventriculoatrial conduction time (110 msec.) suggesting that if A-V nodal bypass tracts exist, they are utilized in an antegrade and retrograde fashion. None of the features of WPW syndrome was present. The mechanism of syncope in the mother and daughter was intermittent third-degree heart block. Both went on to develop permanent complete heart block despite electrophysiologic studies demonstrating 1:1 A-V conduction at extremely rapid atrial pacing rates and both required implantation of permanent pacemakers. The mechanism of syncope in the two brothers was possibly marked sinus bradycardia, but transient complete heart block has not been ruled out. Permanent pacemaker therapy was recommended for both. The nature of the cardiomegaly, which was mild in three patients, is not known. Although not well documented, several maternal relatives have had enlarged hearts, SVT, complete heart block, and syncope.
The submaximal treadmill exercise test is a valuable noninvasive tool for the diagnosis of overt or latent coronary artery disease (CAD). When submaximal heart rates of 80% to 90% of the predicted maximal rates are attained and when ST-segment depression of at least 1 mm is taken as a criterion of ischemia, testing by any of the various exercise protocols with continuous ECG monitoring affords reasonable specificity and sensitivity. The objectives of testing are to (1) diagnose and determine the severity of CAD, (2) assess functional capacity, (3) observe the natural history of disease, (4) evaluate the effects of medical and surgical treatment, and (5) evaluate responses to physical conditioning or to programs directed toward prevention of CAD. Proper precautions and safety standards minimize the risk of exercise testing.
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Spasm of coronary arteries can cause chest pain indistinguishable from classic angina pectoris in patients without atherosclerosis of these vessels or recognizable heart disease. Associated electrocardiographic changes usually correspond to the coronary artery affected and disappear when the attack of pain ends. Sublingual nitrates are excellent agents for the control of the episodic anginal symptoms. There have been scattered reports of myocardial infarction occurring in patients with normal coronary arteries; a role of arterial spasm in these cases in speculative.
Acute mitral regurgitation occurs as a complication of myocardial infarction in perhaps 1% of cases. The characteristic clinical findings include a new systolic murmur occurring in the setting of sudden development of acute congestive heart failure, hypotension, and shock. S3 and S4 gallops and sinus rhythm usually are present, and gross left ventricular or left atrial enlargement usually is not evident radiologically. The immediate and long-term prognoses for patients with acute severe mitral regurgitation are poor without treatment. Although medical therapy can reverse temporarily some of the hemodynamic aberrations, it does not influence survival or eliminate the need for surgical treatment. Surgery consisting of mitral valve replacement and possibly simultaneous coronary revascularization appears to offer some hope in increasing the survival rate among these patients. When acute severe mitral regurgitation is secondary to rupture of chordae tendineae in circumstances other than coronary artery disease, the outlook is not as grim. These patients may show signs and symptoms of congestive heart failure for a few weeks or, at times, many months. Again, sinus rhythm usually is present, with slight left ventircular enlargement, a relatively normal left atrial size, and markedly elevated left atrial and pulmonary arterial pressures. This constellation of findings is indicative of a large mitral regurgitant flow with preservation of left ventricular function and suggests that the patient is likely to benefit greatly from surgical treatment. The prognosis for such patients is much better than it is for the patients with acute mitral regurgitation secondary to coronary artery disease.
Short-term results of aggressive surgical management were compared with results of medical management in forty-three patients with preinfarction angina admitted to the coronary-care unit (CCU) over an 18 month period. These patients were selected from 1,609 consecutive admissions to the CCU because they met strict criteria for preinfarction angina: severe chest pain at rest, ST-segment elevation or depression during pain which subsided rapidly after cessation of pain, and normal serum enzymes (CPK, SGOT, and LDH). Twenty-three patients had coronary angiography, done with operating room and pump standby. One patient, who had total occlusion of the left main coronary artery, died during the study. Twenty-one of the remaining patients were considered surgical candidates, and were treated immediately after angiography with 1 to 3 vein bypass grafts. There was one late postoperative death and, of the 20 survivors, 2 had ECG evidence of acute myocardial infarction and one had mild angina at time of discharge. In contrast, of the 21 patients treated medically, 13 sustained acute MI, resulting in 8 instances of congestive heart failure and 4 cases of ventricular fibrillation. Four patients died in cardiogenic shock. With the use of rigid criteria, a small subgroup of patients with variant angina at high risk of developing AMI has been identified and categorized as having preinfarction angina. Our experience suggests that aggressive surgery immediately following coronary angiography offers a lower incidence of MI, morbidity, and death than does medical management.
A patient with the prolapsed mitral valve syndrome may have no symptoms referable to the heart or, at the other extreme, may have disabling chest pain, severe arrhythmias, and electrocardiographic abnormalities. The syndrome is characterized by a midsystolic click and a late systolic murmur. The mechanism responsible for the valve deformity appears to be related to myxomatous degeneration. Associated ECG abnormalities strongly suggest myocardial disease. The diagnoses is established by echocardiography or cineangiocardiography.
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