Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Young, male, Southeast Asian immigrants living in the United States have a high incidence of unexplained, sudden, nocturnal death. We report the cases of three patients, two Laotians and one Filipino, who were resuscitated and subsequently studied extensively. Each patient was having ventricular fibrillation when first examined by paramedics outside the hospital, and episodes of fibrillation recurred in the early hospital course. Clinical evaluation found no significant coronary atherosclerosis or structural cardiac disease. One patient is asymptomatic after 2 years; the second patient died suddenly at 4 months; and the third is asymptomatic but had inducible ventricular tachycardia on electrophysiologic testing 6 months after resuscitation. The mechanism of sudden death in young Southeast Asian men appears to be ventricular fibrillation. The cause of the arrhythmia is unclear, although in our patients the arrhythmia was not an isolated event; underlying predispositions to further cardiac arrest persisted.
 ...
PMID:Ventricular fibrillation causes sudden death in Southeast Asian immigrants. 673 93

A patient with classic effort and high-grade, fixed proximal coronary atherosclerosis underwent a single saphenous vein graft to a large, dominant right coronary artery (RCA). After being asymptomatic for 1 1/2 years, she had several episodes of rest angina culminating in Prinzmetal angina and ventricular fibrillation. Electrocardiographic changes occurred in the RCA distribution. Symptoms subsided with oral nifedipine therapy. Angiography revealed intact vein graft and coronary circulation. The patient has done well for a follow-up period of 7 months.
 ...
PMID:Coronary artery spasm occurring late after vein graft surgery. 698 10

Sudden coronary death is a syndrome caused by different mechanisms, all of which should be separately considered with respect to preventive measures. Ventricular fibrillation, tachycardia, and complete atrioventricular block were repeatedly observed during ischemic episodes caused by spasm in both the presence and absence of anginal pain. Spasm is, therefore, a potential cause of sudden coronary death. In "variant" angina, which is a reasonably reliable indicator of coronary spasm, arrhythmias occur in about 25% of patients and tend to recur in the same patient. The severity of coronary atherosclerosis in patients who develop severe arrhythmias is quite variable and not dissimilar from patient who do not. Mortality is considerably higher in patients with severe disease, but fibrillation and death can occur also in patients with angiographically normal arteries. In these patients acute and long-term treatment with nitrates and slow channel blockers appears to give remarkable results. Prevention of arrhythmias in patients in whom arrhythmias are secondary to acute ischemic episodes caused by vasospasm should be attempted by preventing vasospasm.
 ...
PMID:Role of coronary arterial spasm in sudden coronary ischemic death. 704 39

Recent clinical and laboratory observations indicate that coronary artery spasm may play a role in the pathophysiology of ischemic heart disease. The majority of patients with ischemic heart disease have coronary atherosclerosis. The prevalence of coronary artery spasm in these patients is unknown. However, current evidence suggests that patients with rest angina have a higher incidence of coronary artery spasm than do patients with reproducible effort angina. Coronary artery spasm may initiate or contribute to acute myocardial infarction, but recent evidence obtained in patients undergoing thrombolytic therapy during the early phases of myocardial infarction suggests that it is not a common occurrence. Although numerous examples of ventricular tachycardia and ventricular fibrillation occur during episodes of coronary artery spasm, the incidence of coronary artery spasm in association with sudden death is unknown. Provocative testing with ergonovine maleate reveals that the highest incidence of provocable coronary artery spasm is found in patients with rest angina. In patients with the syndrome of variant angina, coronary artery spasm is nearly always provocable.
 ...
PMID:Coronary artery spasm: prevalence, clinical significance, and provocative testing. 706 1

Hyperplastic muscle columns encroaching upon the branch mouths of the main coronary arteries were revealed in 1 out of every 5 infants, children, juveniles, adolescents, young adults, mature adults and elderly people. They prevailed at the branching points of the first diagonal and first septal vessels and occupied 1/3 to 2/3 of the coronary wall thickness. The presence of hyperplastic muscle bundles encroaching upon the branch mouths of the main coronary arteries was associated with the absence at the respective sites of branch pads or cushions, intimal connective tissue and atherosclerotic lesions. This peculiar microarchitecture was present in 3 times more frequently in patients who died of coronary heart disease than in subjects who died of non-cardiac causes (30% versus 10%). The existence of a relationship was suggested between the hyperplastic muscle columns encroaching upon the branch mouth of an artery and the infarction area in the myocardium supplied by the respective vessel. Likewise, a relationship seemed to exist between hyperplastic muscle columns encroaching upon the branch mouths of the vessels supplying the sinoatrial and atrioventricular nodes and the electrical instability of the heart, particularly of ventricular fibrillation leading to sudden cardiac death.
Atherosclerosis 1981 Jul
PMID:The hyperplastic muscle columns which encroach upon the branch mouths of the coronary arteries and their relation to coronary heart disease. 725 29

Among 172 cases of coronary artery bypass grafting, 9 cases (5%) revealed severely atherosclerotic ascending aorta. In 3 of the 9 cases, total aortic cross-clamping in the distal anastomoses of saphenous vein graft (SVG) and partial aortic clamp in the proximal anastomoses of SVG were performed. In 1 case with this technique, cerebral infarction was occurred. In 4 cases, total aortic cross-clamping in the distal and proximal anastomoses of SVG was performed. In 2 of these cases with this technique, cerebral infarctions were occurred. Hypothermic circulatory arrest was performed in 2 of the rest. In one case that was predicted to have atherosclerosis of ascending aorta prior to operation, the left internal thoracic artery was anastomosed to the left anterior descending, and SVG to the right coronary artery with hypothermia and ventricular fibrillation. And during the proximal anastomoses of SVG, hypothermic circulatory arrest without aortic clamping was initiated. In another case, atherosclerosis of ascending aorta was noted after aortic cross-clamping. Then the aorta was declamped, hypothermic circulatory arrest was established, the aorta was opened, the diseased segment was resected, and proximal anastomoses of SVG was performed to Dacron patch which was implanted for aortic wall. There were no cerebral infarction in last two patients.
 ...
PMID:[Coronary artery bypass grafting in cases with the atherosclerotic ascending aorta]. 756 18

From pharmacological investigations and clinical studies, it is known that ACE inhibitors exhibit additional local actions that are not related to hemodynamic changes and that cannot be explained only by interference with the renin-angiotensin system by means of an inhibition of ANG II formation. Because ACE is identical to kininase II, which inactivates the nonapeptide BK and related kinins, potentiation of kinins might be responsible for these additional effects of ACE inhibitors. ACE inhibition, concentration, and time dependently increased the formation of NO and PGI2 in cultured endothelial cells of different origin and from different species, including humans. The specific B2 kinin receptor antagonist, icatibant, suppressed the ACE inhibitor-induced increase in endothelial cyclic GMP accumulation index for NO-formation and, in parallel, attenuated the increase in PGI2 release. In renovascular models of hypertension associated with a stimulated renin-angiotensin system (two-kidney, one-clip), blood pressure reduction by ACE inhibitors was attenuated by icatibant, whereas in rats with genetic hypertension with normal to low plasma renin, blood pressure reduction through ACE inhibitors was not affected. In experimental atherosclerosis in rabbits, ACE inhibitors were able to preserve endothelial function and vascular reactivity and to reduce surface involvement. In the balloon denudation model of carotid arteries in rats, it was found that ACE inhibition markedly reduced neointima formation. However, when the ACE inhibitor was given together with icatibant, its effect was significantly blunted. Perfusion with ACE inhibitors induced a reduction of the incidence, as well as of the duration, of ventricular fibrillation and improved cardiodynamics and myocardial metabolism. BK perfusion induced comparable cardioprotective effects. In addition, perfusion with ACE inhibitors markedly increased the outflow of BK and related kinins from isolated rat hearts. The antiischemic effect of ACE inhibitors and BK were abolished by the addition of L-NNA (1 x 10(-6) mol/l) or icatibant (1 x 10(-9) mol/l). Similar results were found in dogs and rabbits with myocardial infarction. BK and related kinins also seem to be involved in preconditioning and remodeling. The effect of ACE inhibition in LVH was investigated in rats made hypertensive by aortic banding. ACE inhibition with ramipril, in the antihypertensive dose of 1 mg/kg/day for 6 weeks, prevented the increase in blood pressure and the development of LVH. A lower, nonantihypertensive dose of the ACE inhibitor (10 micrograms/kg/day for 6 weeks) had no effect on the increase in blood pressure or on plasma ACE activity, but also prevented LVH after aortic banding.4+ off
 ...
PMID:Contribution of kinins to the cardiovascular actions of angiotensin-converting enzyme inhibitors. 778 79

In any discussion of lipids and heart disease it is beneficial from the outset to recognise that at least three different pathological processes may be involved. The first of these is atherosclerosis which involves the deposition of "fat" in the coronary vessels, another is thrombogenesis which describes the formation of blood clots in the coronary vessels, and the third is arrhythmia which refers to disorders in the beating of the heart which may become sufficiently serious to cause sudden cardiac death (SCD). Also it is this disturbance in the rhythmic beating of the heart which is responsible for much of the mortality from 'heart attacks' which occur 'outside-of-hospital' in societies like U.S.A., U.K. and Australia. It is this latter condition of cardiac arrhythmia which is the major concern of this review. Because it is often difficult to differentiate the role of lipids in 'heart disease' in man, it has frequently been assumed that all dietary fatty acids have similar effects on the different processes involved, and many unwarranted generalisations have been made which have led to conflicts of opinion amongst physicians and confusion in the lay public. From the animal studies discussed in this review, it is apparent that dietary fatty acids have an important role to play in determining the vulnerability of the myocardium to develop serious ventricular fibrillation (VF) and potentially lethal cardiac arrhythmia. In general, diets rich in saturated fatty acids promote a state of myocardial vulnerability, whilst diets rich in PUFA significantly diminish the probability of developing lethal disorders in cardiac rhythm when the heart is placed under pharmacological (or emotional) stress, or deprived of sufficient blood flow and supply of oxygen. Very recent experiments with the monounsaturated fatty acid (MUFA) oleic acid clearly demonstrate that, at least in rats subjected to ligation of their coronary artery, this acid is not 'neutral' as has been suggested by some for its role in atherosclerosis, but in fact is indistinguishable from saturated fatty acids in its effect in promoting arrhythmia during either regional ischaemia or reperfusion arrhythmia in this animal model of SCD.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Lipids and cardiac arrhythmia. 787 Jul 38

Anomalous origin of the right coronary artery from the left sinus of Valsalva is a rare congenital anomaly classified as a "minor" anomaly of no clinical importance. Recently, manifestations of myocardial ischemia (angina pectoris, myocardial infarction, nonfatal ventricular fibrillation, sudden death) have been described in patients with this anomaly in the absence of atherosclerosis or other. Sudden death occurs frequently in symptomatic patients and rarely in asymptomatic patients (sudden unexpected death). In this study we report two cases of juvenile sudden death observed in asymptomatic patients with anomalous origin of the right coronary artery from the left sinus of Valsalva. In both cases the sudden death was exertion-related. In case 1 the coronary anomaly was the cause of death, since it was the only significant anatomic abnormality at necropsy; the microscopic findings revealed ischemic lesions only in the myocardium supplied by the anomalous right coronary artery. In case 2 the coronary anomaly was connected to other cardiac and non cardiac diseases (lymphocytic active myocarditis, chronic portitis, encephalitis, medullary adrenalitis). Since these morphologic lesions were extremely slight and there was no adrenal catecholamine damage in the myocardium, we consider negligible their possible role in determining death, which in this case was induced by the congenital coronary anomaly. The cardiac microscopic findings, also in this case, revealed ischemic lesions in the myocardium supplied by the anomalous right coronary artery.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Anomalous origin of the right coronary from the left sinus of Valsalva. A possible cause of juvenile sudden death]. 817 67

The authors summarize the early results of coronary angioplasty in 234 patients, with special emphasis on complications. The follow-up group included 182 men (77.8%) and 52 women (22.2%) with a mean age of 52 (34-74) years. Single-artery involvement prevailed (216 patients, 92.3%); multiple artery involvement was diagnosed in 18 patients (7.7%). Overall, dilatation was performed in 273 stenoses; of this number, 213 procedures were successful (78.0%). The primary success rate in the whole group was 76.9% (180/234). The highest success rates were attained in concentric stenoses (88.8%), the lowest ones in complete occlusions (53.8%). Complications were present in 36 patients (15.3%), of this number 14 patients (5.9%) developed acute arterial occlusion; the complications were less severe in 22 patients (9.4%). Of the 14 patients with acute occlusion, eight (3.5%) developed severe complications. One female patient (0.43%) died, one (0.43%) had emergency surgery, and six (2.6%) developed uncomplicated acute myocardial infarction. Perfusion was restored by multiple dilatation in four patients; arterial occlusion, with good collateral circulation, did not result in myocardial infarction in two. Other complications were less severe and had no sequelae including, most often, arterial spasm (3.4%), large dissection demonstrated by angiography (2.6%), protracted hypotension (0.8%), and ventricular fibrillation in one case (0.43%). The article also considers the factors raising the risk of severe complications of coronary angioplasty, and the potential for their prevention and treatment. Coronary angioplasty, employed in an increasing number of patients with symptomatic stenosing atherosclerosis of the coronary arteries, is an effective method successful in 85-95% of patients. The complication rate, while low, is not absolutely negligible.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Early results and complications of percutaneous transluminal coronary angioplasty]. 850 Feb 99


<< Previous 1 2 3 4 5 Next >>