Coronary occlusion in early myocardial infarction.
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Biomedical subjects
Publications and source records attributed to R C Pasternak.
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Twelve autopsy human hearts were submitted to coronary angiography and coronary arterial balloon angioplasty. The effect of angioplasty was determined by follow-up coronary angiography as well as gross and microscopy inspection of the coronary arteries dilated. Fifty-four dilations were performed in 24 coronary arteries. Angiographically 50 of the 54 dilations resulted in a mean (+/- standard deviation) increase in luminal diameter ranging from 1.9 +/- 0.9 to 2.7 +/- 0.8 mm. Failure to increase luminal size was usually related to a predilation coronary diameter greater than that of the inflated angioplasty balloon. Dilation resulted in mural disruption with intimal or medial tears, or both, in 65 percent of arteries dilated. Disruption was more frequent in arteries with atherosclerosis and calcification. The mechanism of luminal enlargement in coronary angioplasty may be focal damage to the arterial wall with intimal or medial splitting as opposed to plaque compression as initially suggested.
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Among 3,242 coronary angiograms performed from November 1972 through October 1975 at the Massachusetts General Hospital, 175 patients had normal coronary arteries or luminal narrowings of less than 30 per cent. All patients were studied for chest pain, and none had experienced prior myocardial infarction. Subsequent information was available in 159 patients over a mean follow-up period of 42.7 months. There were no deaths, and only one myocardial infarction occurred during this period. However, among the patients followed, continued chest pain with episodes occurring at least once monthly was present in 54 per cent. In addition, 17 per cent of all patients required subsequent hospitalization and 44 per cent continued to receive antianginal medication. Nearly half of the group (46 per cent) suffered some limitation of activity, and 22 per cent stated that they had either changed jobs or stopped work because of chest pain. Continuing chest pain was significantly more common in women and in patients who had experienced chest pain for more than one year before angiography. However, typicality of chest pain for angina or the occurrence of electrocardiographic changes of ischemia prior to angiography did not predict continued chest pain during the follow-up period. Thus, although mortality and morbidity are low in this group of patients, the syndrome of chest pain with angiographically insignificant coronary artery obstruction has an important impact on the lives of a majority of those affected.
Percutaneous coronary transluminal angioplasty is currently being proposed as a possible treatment for some patients with significant coronary arterial lesions. In this study scanning electron microscopy was used to assess the morphologic changes caused by the angioplasty balloon catheter in normal canine coronary arteries. Balloon inflation uniformly caused endothelial denudation with virtually immediate dense platelet adhesion to the subendothelial matrix. This platelet adhesion was unaffected by pretreatment with aspirin (35 mg/kg body weight) or heparin (2,000 units). However, intravenous administration of low molecular weight dextran almost completely prevented platelet adhesion to the exposed subendothelial connective tissues. It is concluded that even in normal canine coronary arteries (1) loss of endothelium is seen after transluminal angioplasty; (2) this endothelial damage stimulates platelet adhesion and thrombus formation; and (3) the immediate layering of platelets can be prevented by administration of low molecular weight dextran.
The morphologic consequences of transluminal angioplasty of stenotic atherosclerotic coronary arteries are unknown. This study describes the production of aortoiliac atherosclerosis in rabbits and reports the morphologic changes after transluminal angioplasty of stenotic arterial lesions. Atherosclerotic lesions were evaluated angiographically before and after transluminal angioplasty and were studied histologically and by electron microscopy after angioplasty. Moderatley stenotic aortic segments showed denudation of endothelial cells and deposition of a carpet of platelets enmeshed in fibrin. Medial and intimal compression were not seen. Intimal plaque disruption and splitting of atheromatous plaques were observed in more stenotic vessels where dilatation during angioplasty is relatively greater. Transluminal angioplasty, therefore, acutely causes desquamation of endothelial cells and superficial plaque elements, splitting of atheroma and subsequent deposition of platelets and fibrin in the area of angioplasty. This experimental model may be useful to evaluate the morphologic changes after angioplasty and might be used in further studies to determine the long-term pathophysiologic changes after transluminal angioplasty.
The effects of direct intracoronary injection of meglumine diatrizoate (RENOGRAFIN) on regional myocardial contractility were studied in 11 open-chested dogs. The left anterior descending or circumflex artery was cannulated selectively from the ascending aorta and the changes in myocardial contractile force and its first derivative were measured by an epicardial strain gauge sutured to the myocardium supplied by the cannulated artery. The myocardium perfused by the non-cannulated artery served as the control area. Direct intracoronary injection of meglumine diatrizoate, 1 ml, caused regional depression of myocardial function, with a significant decrease in contractile force and its first derivative in the study area; there was no change in the control area, nor were there changes in the first derivative of left ventricular pressure, heart rate or systemic blood pressure. There was no additive depressant effect after multiple injections. Local pretreatment with hydrocortisone (4 mg/kg, by slow intracoronary infusion) ameliorated the myocardial depressant effect of meglumine diatrizoate so that there was a smaller decrease in contractile force and its first derivative. The results may have clinical significance in patients undergoing coronary arteriography.
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Fifty-four patients with variant angina are described. They are divided into patients without hemodynamically (less than 50%) important coronary artery lesions (Group 1), patients with intermediate (greater than or equal to 50% and less than 90%) fixed obstruction (Group 2A), and patients with high grade (greater than or equal to 90%) fixed obstruction (Group 2B). Inferior ischemia occurred significantly more often in Group 1 (90% versus 33%. p less than 0.001), and exertional angina was more frequent in Group 2 (70% versus 36%, p less than 0.05). Maximum medical therapy with propranolol and nitrates failed to control angina in 55% of Group 1, 69% of Group 2A, and 63% of Group 2B. Twelve patients underwent intra-aortic balloon pumping (IABP), and in 10 there was complete control of variant angina. A total of 35 Group I patients underwent coronary artery bypass grafting (CABG), with a 2.9% mortality rate in patients without preoperative cardiogenic shock. Of these patients, 55% in Group 2A and 73% in Group 2B experienced marked improvement in their angina status. Therefore, we currently recommend bypass grafting for medically intractable variant angina in those patients with severely stenotic, fixed atherosclerotic lesions.
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In a patient with endocarditis due to Candida tropicalis echocardiograms from mitral valve vegetations were found to mimic the typical pattern of a left atrial myxoma. A mass was shown occupying the mitral orifice posterior to the anterior mitral leaflet; densities also appeared in the left atrium. Though these echocardiographic findings were consistent with the diagnosis of a left atrial myxoma, there were other distinctive differential diagnostic features. Other diagnostic possibilities must, therefore, be considered in the interpretation of echocardiograms which suggest left atrial tumour.
BACKGROUND: Hospitalization may be an opportune time to change smoking behavior because it requires smokers to abstain from tobacco at the same time that illness can motivate them to quit. A hospital-based intervention may promote smoking cessation after discharge. METHODS: We tested the efficacy of a brief bedside smoking counseling program in a randomized controlled trial at Massachusetts General Hospital, Boston. The 650 adult smokers admitted to the medical and surgical services were randomly assigned to receive usual care or a hospital-based smoking intervention consisting of (1) a 15-minute bedside counseling session, (2) written self-help material, (3) a chart prompt reminding physicians to advise smoking cessation, and (4) up to 3 weekly counseling telephone calls after discharge. Smoking status was assessed 1 and 6 months after hospital discharge by self-report and validated at 6 months by measurement of saliva cotinine levels. RESULTS: One month after discharge, more intervention than control patients were not smoking (28.9% vs 18.9%; P=.003). The effect persisted after multiple logistic regression analyses adjusted for baseline group differences, length of stay, postdischarge smoking treatment, and hospital readmission (adjusted odds ratio, 2.19; 95% confidence interval, 1.34-3.57). At 6 months, the intervention and control groups did not differ in smoking cessation rate by self-report (17.3% vs 14.0%; P=.26) or biochemical validation (8.1% vs 8.7%; P=.72), although the program appeared to be effective among the 167 patients who had not previously tried to quit smoking (15.3% vs 3.7%; P=.01). CONCLUSIONS: A low-intensity, hospital-based smoking cessation program increased smoking cessation rates for 1 month after discharge but did not lead to long-term tobacco abstinence. A longer period of telephone contact after discharge might build on this initial success to produce permanent smoking cessation among hospitalized smokers.