Progression Of Coronary Arteriosclerosis Research Articles

The influence of obesity on progression of coronary arteriosclerosis and clinical course after ST elevation acute myocardial infarction treated with primary coronary interventions

Evaluation of influence of obesity on the coronary atherosclerosis development and clinical outcome in patients with STEMI treated by PCI with BMS implantation. 82 patients (64 men) treated with PCI within 6 hours from 1st STEMI. Three groups of pts were formed according to BMI. Based on coronary angiography number of significant stenoses (NSS), number of stenosed coronary arteries (NSA), and sum of significant stenoses (SSS) were calculated. Echocardiography examination was performed 3 days and 6 months after STEMI. Serial evaluation of TnI, CK, CKMB was performed after admission, and serum BNP was assessed after 2 days, 1 and 6 months after STEMI. Obese patients revealed higher values of NSA, NSS and SSS than patients with normal BMI and overweight. There were no differences of BNP, maximal values and AUC of CK, CKMB, TnI and echocardiographic parameters between all groups whereas decrease of BNP during follow-up correlated with BMI. Results of our prospective study indicate that in obese patients, there is a significantly greater number of atherosclerotic lesions in coronary arteries found during PCI, as compared to those with normal body weight or overweight. We proved that overweight and obesity did not result in significantly greater damage to the myocardium and left ventricular dysfunction, both in the acute phase and 6 months after myocardial infarction treated with primary coronary intervention, as compared to those with normal body weight. In addition correlation was found between BNP concentration profile and body mass index in the 6-month follow-up after STEMI treated with PCI and bare metal stent implantation.

Metabolism of hepatocyte growth factor in the heart in patients with coronary artery disease: implication for coronary arteriosclerosis.

HGF, one of endothelium-specific growth factors, might contribute to the repair process of vascular endothelial cell damage, suggesting that serum HGF concentration may be elevated in patients with arteriosclerosis. However, the cardiac metabolism of HGF has not been examined in patients with coronary artery disease (CAD). We examined the levels of hepatocyte growth factor (HGF) in the coronary circulation and its correlation with the severity of arteriosclerosis in patients with CAD. We measured serum HGF concentration obtained from the coronary sinus (CS) and ascending aorta (AA) in patients with atherosclerotic CAD (Group E, n = 33) or vasospastic angina (Group V, n = 26), or normal control subjects (Group N, n = 12). In Group E, the severity of coronary artery stenosis was evaluated using the Gensini's score. Serum HGF concentrations (ng ml) in the CS were 0.112 +/- 0.008 in Group E (p < 0.001 vs. Group V, p < 0.001 vs. Group N), 0.197 +/- 0.012 in Group V (p = 0.031 vs. Group N), and 0.245 +/- 0.021 in Group N. Serum HGF concentrations in the AA were 0.282 +/- 0.014 in Group E (p = 0.045 vs. Group V, p = 0.021 vs. Group N), 0.246 +/- 0.012 in Group V, and 0.237 +/- 0.009 in Group N. Serum HGF extraction in the heart (HGF in the AA-HGF in the CS) in Group E (0.170 +/- 0.018) was significantly higher compared with in Group V (0.049 +/- 0.011) or Group N (0.008 +/- 0.005). There was a significant negative correlation between the severity of coronary arteriosclerosis and serum HGF concentration in CS (r = -0.66, p < 0.001), and a significant positive correlation between the severity of coronary arteriosclerosis and HGF extraction in the heart (r = 0.75. p < 0.001). We conclude that the difference of HGF levels between CS and AA in patients with CAD are decreased, and extent of decreases in HGF levels correlates with the severity of coronary arteriosclerosis. The abnormality of HGF metabolism in the heart may contribute to the progression of coronary arteriosclerosis.

Changes in the morphology and components of the coronary arteries during the progression of coronary arteriosclerosis following cardiac transplantation in rats

In order to examine the changes in coronary artery morphology following cardiac transplantation, the intimal and medial areas and vascular components were measured 30 and 60 days postoperatively in rats receiving both iso- ( n=5, each time) and allotransplantations ( n=7, each time). Although cyclosporine A was administered intramuscularly (10 mg/kg per day) for 20 days following transplantation, graft rejection progressed gradually in the allotransplanted group. There were no clear changes in the intimal or medial areas following transplantation in the isotransplanted group. The intimal area of the coronary arteries in the allograft group was significantly thicker 30 and 60 days following transplantation, while the medial area of the coronary arteries in this group was significantly thinner than that of the isotransplantation group at these same time points. In the thickened intimal areas in the allotransplantation group, only the density of smooth muscle cells was higher following transplantation. In the thinned medial areas in the allotransplantation group, the densities of the smooth muscle cells and collagen were less than those in the isotransplantation group. These changes suggest that following transplantation, smooth muscle cells proliferate in the intimal areas, while smooth muscle cells and collagen are degraded in the medial areas.

Myocardial infarction at a young age (under 40 years).

Coronary morphology, risk factors, long-term prognosis, and progression of coronary arteriosclerosis were investigated in 679 (649 mean and 30 women) post-infarction patients under 40 years of age. These patients represented 80% of 844 MI patients under 40 who were referred to our hospital in the years 1973-1980; 20% had refused coronary angiography; 465 patients were followed up for 1-7 years (mean 3.5 years). In 164 patients, a second coronary angiography was performed 3.8 years after the first angiogram, which was done an average 3 months after the acute episode. The main results were as follows: 8.4% of the patients had zero-vessel disease and 3.7% had a normal coronary angiogram. The majority had single-vessel disease (57.3%). The prevalence of zero-vessel disease decreased with age while that of multivessel disease increased. With increasing vessel involvement, the prevalence of hypercholesterolemia, hypertriglyceridemia, and hypertension increased. A history of smoking was equally common in patients with zero-, single-, double-, and triple-vessel disease. In women the combination of smoking and the use of oral contraceptive drugs was frequently seen. In one-quarter of the zero-vessel disease patients, the infarction occurred during unusually intense physical exercise. The statistical analysis of the survival data using the proportional hazards model (univariate analysis) showed the variables heart volume/body wt., ventricular arrhythmias, PCP at rest, PCP max, work capacity, ventricular function, and number of diseased vessels to be of prognostic importance. Multivariate analysis using this model revealed the following independent variables to be relevant to prognosis: heart volume/body wt., ventricular arrhythmias, ventricular function, and number of diseased vessels. After an average of 3.8 years since the first coronary angiography, 28.6% of the patients showed a significant progression of coronary arteriosclerosis (at least two degrees of stenosis according to the AHA classification). In the subgroup of patients with multilocular disease in the first angiogram, progression was 10 times as frequent as in a group with initial unilocular disease (34.3% vs 3.6%). Patients with progression had continued to smoke significantly more often than patients without progression (38.4%) vs 14.5%). Regression of coronary angiographic findings was significantly more frequent in the group of patients with initial unilocular disease than in those with multilocular disease in the first angiogram (28.6% vs 10.6%). Regression might be explained as recanalization and organization of a thrombus.(ABSTRACT TRUNCATED AT 400 WORDS)

Coronary heart disease: pathlogy (author's transl)

The review deals first with the importance of the risk factors for coronary heart disease, the progression of coronary arteriosclerosis and the location of atherosclerotic lesions. The areas of blood supply to the coronary arteries and the effects of coronary insufficiency in the myocardium are discussed. Finally the aneurysm and the morphologic changes in aortocoronary venous bypass are described.

Pathology of coronary arteriosclerosis ∗

The heart and coronary arteries from 1,500 American soldiers killed in action in Korea and from 1,500 routine autopsies in the Arlington Community Hospital, Arlington, Virginia, have been studied to determine the pathogenesis and progression of coronary arteriosclerosis. In addition, autopsy material from 114 cases of Japanese natives was also available. Certain observations were also made from 600 autopsies performed at the Board of Health Laboratory, Gorgas Hospital, Ancon, Canal Zone. The probable alteration in the process of natural diffusion within the arterial wall, primarily occurring within the intima, seems to offer an important clue to the fundamental pathogenesis of atherosclerosis. Sites of predilection for the lesion seem to be initiated at points of increased hemodynamic stress but are undoubtedly complicated by other intrinsic anatomic and physiologic factors which exert their influence in rather dramatic contrast between the two sexes and, in the case of the female subject, at different ages relative to the activity of her reproductive period. This observation, regarded as factual by most investigators, is significant and challenging. Points of hemodynamic stress in the arterial system of the male and female subject should, in the absence of predilection for atherosclerotic lesions in the two sexes, coincide. Eventually they do, but for puzzling reasons the site of predilection in the female subject does not exhibit clinically significant atherosclerotic lesions during her active reproductive period, a time during which she may have one to several episodes of hypercholesteremia associated with pregnancy. Arteriosclerotic lesions apparently accelerate with the decline in the reproductive period. This seems to be the single constant among the many variables observed in the pathogenesis of coronary arteriosclerosis. Statistics are presented pointing out the differences in the incidence of coronary disease between the white American, the American and African Negroes, and the Japanese. The distribution of sudanophilic material in the coronary arteries of the Japanese is offered as one of the possible morphologic expressions of dietary differences among the races. The fact that atherosclerotic lesions in the epicardial segments of the coronary arteries cause significant luminal narrowing in a majority of young white adult American male subjects examined at postmortem, regardless of the cause of death, brings to medical attention one of the most serious cardiovascular problems in the United States today.

CLINICAL OBSERVATIONS IN CASES OF MASSIVE MYOCARDIAL INFARCTION

MYOCARDIAL infarction is a dramatic episode in the course of coronary artery disease, but it is often thought of in terms of a disease entity with its own course, prognosis and treatment. With the occurrence of myocardial infarction, a new factor is introduced into the course of coronary artery disease with myocardial ischemia, namely, gross and irreparable destruction of a portion of the cardiac muscle. This damage to the myocardium determines the immediate prognosis and the ultimate outcome entirely independently of the degree and progression of coronary arteriosclerosis. Thus, the size of the area of the destroyed muscle is one of the important factors in the prognosis, yet little investigative work has been done in estimation of the size of a myocardial infarct during life. In terms of ordinary clinical thinking, a severe attack of pain with fully developed clinical signs of myocardial infarction is usually considered as evidence of