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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The usefulness of end-systolic measures of left ventricular performance as a load-independent method of assessing of ventricular contractility has been studied in intact, conscious dogs. The end-systolic pressure-chamber diameter (P-D) relation was shown to be linear, unaltered by preload changes, and shifted in a parallel fashion by inotropic stimulation, whereas the end-systolic pressure-volume relation appeared to increase in slope with increased contractility. A simplified measure of end-systolic relations that does not require measurement of chamber volume or diameter, the end-systolic pressure-wall thickness ( WTh ) relation, was also linear and shifted with acute changes in inotropic state. During regional ischemia, the regional end-systolic WTh relation also may provide a relatively load-independent means of detecting regional depression of myocardial contractility. With chronic pressure overload hypertrophy in dogs, the end-systolic P-D relation was markedly shifted upward and to the left, which indicates hyperfunction of the left ventricle; however, end-systolic wall stress-diameter relations were identical before and after the development of hypertrophy, which suggests that myocardial contractility was unaltered. These findings and clinical studies of mitral regurgitation imply that for assessing resting left ventricular contractility in certain chronic conditions, the use of wall stress rather than pressure may be appropriate in the end-systolic framework. Further experimental studies are needed in the intact circulation to better characterize end-systolic relations before their full potential in the clinical setting can be realized.
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PMID:Applications and limitations of end-systolic measures of ventricular performance. 623 74

The prerequisite in establishing the indication for coronary arteriography is low mortality and morbidity of the procedure. Mortality is about 1%, major complications are myocardial infarction (1.5 to 2%) and cerebral embolism (less than 1%). These low complication rates are generally achieved only in institutions which perform at least 400 procedures per year. Coronary arteriography is indicated in the following groups of patients: patients with angina pectoris aged below 45; patients over 45 with sudden worsening of angina, angina pectoris uncontrolled by medication (impaired quality of life) and cases where there is objective evidence of severe ischemia on exercise though angina is mild; recurrence of angina or positive stress ECG after myocardial infarction; following an episode of unstable angina; following resuscitation due to ventricular fibrillation; suspected Prinzmetal angina; postinfarction aneurysm with signs of heart failure; candidates for valve surgery aged over 45. Coronary arteriography is also performed to evaluate the result of bypass surgery, in patients with unclear diagnosis exposed to occupational hazards, and in acute myocardial infarction (thrombolysis, ventricular septal rupture, acute mitral regurgitation). The main indications for radioisotope studies (Tl-201 myocardial scintigraphy and radionuclide angiography during dynamic exercise) are detection and localization of ischemic zones and scars in patients with known coronary disease, and evaluation of the result of coronary artery bypass surgery. Less frequent indications are, today, atypical chest pain and uninterpretable ECG, and asymptomatic patients with abnormal stress ECG. 2-d echocardiography is the most widely used noninvasive technique for qualitative assessment of regional wall motion disorders at rest. 3800 coronary arteriographies are performed yearly in the public hospitals of Switzerland.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Indications for coronary angiography and other special studies]. 660 28

The main and most attractive surgical measure in acute coronary disease is emergency revascularisation of acute ischemia. As far as unstable angina is concerned, the recommendations of the National Cooperative Study Group are more or less universally accepted, which means that emergency revascularisation is reserved for patients in whom stabilisation of angina with vigorous medical treatment is unsuccessful. On the other hand, it has been shown that a large proportion of patients in whom unstable angina had been successfully stabilized subsequently suffered from severe chronic angina. The author therefore recommends performing coronarography in all younger patients within a few days. If left main stem or three-vessel disease is documented by this investigation, aortocoronary bypass should be performed during the same hospitalisation. In cases with isolated proximal stenosis of the left anterior descending artery, transluminal dilatation should be considered. The author's own results confirm the general experience that revascularisation for unstable angina does not involve elevated risk. After established acute infarction, the role of surgery is confined to treatment of severe mechanical complications of infarction (acute aneurysm, ventricular septal defect, subvalvular mitral insufficiency) and aortocoronary bypass for postinfarction angina. The author's results show that early and late mortality are rather high, though a good late result can be achieved in about 50% of the cases. However, in view of the poor prognosis under conservative treatment, even this modest rate of success seems acceptable.
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PMID:[Surgical treatment of acute coronary heart disease]. 661 Sep 37

DT, a 63-year-old white male with insulin-dependent diabetes mellitus and severe peripheral vascular disease, was admitted with a five-day history of vague abdominal pain and diarrhea. On the day of admission he vomited three times, was noted to have a bloody stool, and came to the emergency room. DT denied hematemesis, fever, or chills. He had bilateral leg amputations and had sustained three myocardial infarctions, the last one 15 months before this admission. He had never experienced symptoms of abdominal angina. Of significance was his history of congestive heart failure, mitral regurgitation, and atrial fibrillation. His medications on admission included digoxin 0.25mg per day, furosemide 40mg per day, and NPH insulin 15 units per day. On admission to the hospital his oral temperature was 38 degrees C, pulse was 90/min, respiratory rate was 24/min, and blood pressure was 134/80mmHg. Abdominal examination revealed a distended abdomen with hypoactive bowel sounds and mild tenderness. Chest x ray revealed cardiomegaly. The electrocardiogram demonstrated atrial fibrillation. A plain film of the abdomen was positive for gallstones and edema of the bowel wall (thumb-printing). Laboratory results included blood urea nitrogen 48mg%, creatinine 1.2mg%, hemoglobin 18g/dl, and hematocrit 52.9%. White blood cell count was 11,900 cells/cc with 33% polymorphonuclear leukocytes, 47% bands, 8% lymphocytes, 11% monocytes, and 1% atypical lymphocytes. The prime considerations for differential diagnosis were mesenteric ischemia and infectious gastroenteritis. While it was appreciated that mesenteric ischemia, if present, might warrant surgical intervention, the risk of anesthesia itself in this patient was felt by his attending physicians to exceed 30%. Furthermore, the clinical findings were only "suggestive" of mesenteric eschemia. They were certainly not "diagnostic." In view of this dilemma, a consultation with the Division of Clinical Decision Making was requested.
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PMID:Abdominal pain, atherosclerosis, and atrial fibrillation. The case for mesenteric ischemia. 716 38

From 1972 to September, 1979, 20 patients underwent transplantation of the anomalous left coronary artery to the aorta, either directly or via a graft. Correction of ischemia-induced mitral insufficiency was associated in eight patients and a postinfarction left ventricular scar was excised in 12. Operative mortality was high among patients under 1 year of age (4/5). Among older children it was 15%. There were not late deaths among patients surviving the operation (mean follow-up 3 years). All but one had marked clinical improvement and reduction of cardiomegaly. Eleven patients underwent angiographic control, with a patent graft or anastomosis demonstrated in every case. Operation is advocated for patients over 1 year of age. The best treatment of symptomatic infants remains controversial.
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PMID:Surgical treatment of anomalous origin of the left coronary artery in infancy and childhood. Early and late results in 20 consecutive cases. 727 32

To clarify the types and frequency of myocardial fibrosis and vascular lesions caused by different types of the rheumatic valvular disease, 41 autopsied hearts with rheumatic valvular lesions were examined and the following results were obtained. As to myocardial fibrosis, 1) perivascular fibrosis, caused mainly by perivascular inflammation and partly by myocardial strain, varied in grade according to the types of the valvular disease, i.e., most severe in mitral regurgitation (MR) and combined valvular disease (CVD) and least in mitral stenosis (MS); 2) Aschoff's nodes: 3 typical and 8 atypical cases were found; 3) perimycial fibrosis due to myocardial strain: most severe in MR and CVD and least in MS; and 4) irregular patchy fibrosis, caused mainly by myocarditis and partly by ischemia, was noticed in all types of the valvular disease. As to vascular lesion, 1) angitis was found in 7 cases and most frequently in MR; and 2) thickening of the intima and media was found in all types of valvular disease. Thus, myocardial fibrosis and vascular lesion varied according to the types of valvular disease, and not only hemodynamic changes but also myocardial fibrosis and vascular lesions might determine the prognosis of the valvular disease.
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PMID:Histopathological studies on the myocardial fibrosis and vascular lesion of rheumatic valvular disease. 732 Nov 53

Mitral valve prolapse (MVP), which occurs in about 3% of adults, is usually a primary, dominantly inherited condition. MVP may be diagnosed by auscultation of a mid-systolic click and late-systolic murmur that move dynamically with postural maneuvers. M-mode echocardiography confirms MVP by demonstrating late-systolic prolapse and two-dimensional echocardiography reveals leaflet billowing into the left atrium. Echocardiography identifies severe forms of MVP by documenting significant mitral regurgitation, enlargement and thickening of the mitral leaflets and annulus, and loss of leaflet apposition. In contrast to early reports, true "MVP syndrome" as revealed by controlled studies consists of low body weight and blood pressure, minor skeletal abnormalities, orthostatic hypotension, palpitations, and mitral regurgitation that is usually mild. Complications of MVP include progressive mitral regurgitation, infective endocarditis, orthostatic syncope, and possible risks of neurologic ischemia and arrhythmic sudden death. Risk factors we have identified for complications among patients with MVP include older age, male gender, the presence of mitral regurgitation, and possibly, higher weight and blood pressure. The cumulative risk of all complications of MVP by age 75 is from 5% to 10% for affected men and 2% to 5% for affected women. Patients with MVP who have neither a murmur nor Doppler evidence of mitral regurgitation may be reassured that their condition is benign. For other patients with MVP we have shown that oral antibiotic prophylaxis is cost-effective. The presence and severity of mitral regurgitation govern the frequency and intensiveness of follow-up.
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PMID:Recent developments in the diagnosis and management of mitral valve prolapse. 778 75

Mitral valve prolapse (MVP) is usually a primary, dominantly inherited condition. Diagnosis may be made by auscultation of a midsystolic click and late-systolic murmur that move dynamically with postural maneuvers. Echocardiography confirms the diagnosis by demonstrating M-mode late-systolic prolapse and 2-D leaflet billowing into the left atrium. More severe forms of MVP can be detected echocardiographically by documentation of significant mitral regurgitation, enlargement and thickening of the mitral leaflets and anulus, and loss of leaflet apposition. In contrast to earlier reports, the true "MVP syndrome" consists of low body weight and blood pressure, minor skeletal abnormalities, orthostatic hypotension, palpitations and mitral regurgitation of variable degree. Complications of MVP include progressive mitral regurgitation, infective endocarditis, and possible risk of neurologic ischemia, arrhythmic sudden death, and orthostatic syncope. Risk factors for complications among MVP patients include older age, male gender, the presence of a mitral regurgitant murmur, and, possibly, higher weight and blood pressure. MVP patients with neither a murmur nor Doppler evidence of mitral regurgitation may be reassured that their condition is benign. For other MVP patients, the presence and severity of mitral regurgitation govern the frequency and intensiveness of needed follow-up.
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PMID:Mitral valve prolapse. 782 19

We recently encountered a patient with mitral insufficiency, accompanied by PN (polyarteritis nodosa), who developed a cardiac rupture immediately after a mitral valve replacement. The patient was a 60-year-old woman. After she was diagnosed as having mitral stenosis and insufficiency in 1968, the patient developed congestive heart failure and underwent repeated hospital admissions and discharges. In 1989, she was diagnosed as having PN and began to receive a high-dose steroid therapy (prednisolone; total dose 5245 mg). Because of transient brain ischemia and exacerbation of the symptoms of heart failure, the patient underwent mitral valve replacement on December 19, 1991. For anesthesia, oxygen, fentanyl, midazolam and vecuronium were administered. During surgery, catecholamine, nitroglycerin and prostaglandin E1 were continuously infused intravenously. The patient was weaned smoothly from the cardiopulmonary bypass. The operation was completed in about 6 hours. Her postoperative course was satisfactory until she suddenly developed left ventricular rupture and died 6 hours after surgery. The rupture seemed to be attributable to a weakening of the myocardial wall following long-term, high-dose steroid therapy, and to myocardial degeneration caused by PN-associated necrotizing vasculitis of myocardial arterioles.
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PMID:[Anesthetic management of a patient with polyarteritis nodosa who suddenly developed cardiac rupture after valve replacement]. 790 39

Nitrates are commonly used in the therapy of congestive heart failure (CHF). They exert beneficial hemodynamic effects by decreasing left ventricular filling pressure and systemic vascular resistance while modestly improving cardiac output. The improvement in left ventricular function caused by nitrates is the result of combined reduction in outflow resistance and mitral regurgitation, while decreased pericardial constraint and subendocardial ischemia may also contribute to the process. With continuous nitrate administration, complete arterial tolerance develops, while venous tolerance appears to be only partial. The major mechanism of tolerance is loss of vascular smooth muscle sensitivity to nitrates. An increase in total blood volume occurring during the first few hours of an acute administration may partly contribute to tolerance. The importance of reflex neurohumoral activation is controversial; although it may contribute to tolerance in CHF, its role does not appear to be major. Chronic continuous nitrate therapy in CHF improves submaximal and maximal exercise tolerance. In combination therapy with hydralazine, isosorbide dinitrate reduces mortality, although to a lesser extent than the angiotensin converting enzyme inhibitor enalapril. Intravenous or sublingual nitrates are first-line agents in the therapy of acute pulmonary edema. In severe CHF, refractory to standard medical therapy, a short course of intravenous nitroglycerin, with or without inotropic agents, can help break the vicious spiral of CHF. Because tolerance occurs without nitrate-free intervals and until an optimal schedule of administration is determined, it makes good sense to include a nightly nitrate-free interval when prescribing nitrates for CHF in order to maintain maximal benefit during the hours of activity.
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PMID:Nitrates in congestive heart failure. 794 67


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