Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Conventional plasma isoenzyme and enzyme values usually are normal during the first few hours of acute myocardial infarction. Thus definitive diagnosis may be delayed. We have shown recently that infarction in dogs can be detected within 1 hr after coronary occlusion by analysis of relative activities of MM creatine kinase (CK) isoforms in plasma. Isoforms of MM CK evolve through posttranslational modifications in plasma of the form released from tissue (MMA) to MMB and MMC. In this study we quantified changes in isoform profiles in the first available plasma samples from patients with evolving myocardial infarction, from patients with angina, and from normal subjects. In the 26 control subjects, the ratio of MMA to MMC was 1.09 +/- 0.4 (SE) (range 0.31 to 3.1; upper limit of normal [defined as the mean plus 2 SD] 2.5). In the seven control patients with coronary artery disease, the ratio of MMA to MMC was 1.3 +/- 0.3 with a range of 0.5 to 2.5. In contrast, among the 28 patients with acute myocardial infarction, the ratio of MMA to MMC in the first available plasma sample averaged 14.6 +/- 4.5 (p less than .01 compared with both control groups). First available samples were obtained 3.9 +/- 0.4 hr after the onset of pain. In 24 of 28 patients (86%) the ratio of MMA to MMC was greater than 2.5.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diagnostic changes in plasma creatine kinase isoforms early after the onset of acute myocardial infarction. 370 69

In order to discuss the mechanism of onset in myocardial infarction (MI), clinical cases were reviewed and various clinical findings were analyzed according to the premise that the onset of MI requires both a predisposition and a trigger. The majority of subjects did present conditions that constituted predispositions for MI, including a history of angina pectoris (especially unstable angina), poor therapeutic results for angina pectoris, organic stenosis of the coronary artery, life changes, and overwork. Patients with multiple factors tended to develop MI without a definite trigger, i.e., onset during sleep or rest whereas, in patients with fewer predisposing factors, it was obvious effort, excitation or stress that triggered MI. However, not a few of the patients presented with no organic stenosis of the coronary artery or no history of angina pectoris. There were patients without ST segment elevation at onset of MI, and patients in whom ST elevation was recorded after onset. These findings suggest the existence of mechanisms other than coronary occlusion in onset of MI. Occlusion of the coronary artery distributed to the infarct region occurred frequently among patients with delayed CPK efflux as well as prolonged chest pain and ST segment elevation. These lines of evidence suggest extension of infarction due to secondary coronary occlusion.
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PMID:Evaluation of clinical factors involved in onset of myocardial infarction. 372 78

Twenty-four of 96 patients with unstable angina exhibited transient ST-T abnormalities in anterior electrocardiographic leads at rest combined with severe subtotal stenosis (80% to 95% narrowing) of the proximal left anterior descending artery (LAD). This entity is termed staccato LAD occlusion to signify the probable pathophysiology responsible for the patients' repeated episodes of ischemic cardiac angina. Although staccato LAD occlusion represents a minority of patients hospitalized with unstable angina, it includes most who suffer cardiac complications. Among patients treated medically, 10 of 16 with staccato LAD occlusion developed anterior myocardial infarction, whereas cardiac complications occurred in only three of the remaining 50 patients with unstable angina during the 4-month follow-up period (p less than 0.001). Medical treatment of staccato LAD occlusion should be directed primarily against coronary occlusion. Considering the high risk of myocardial infarction, until reliable methods for preventing the threatened occlusion are demonstrated, urgent coronary bypass surgery seems warranted for these patients.
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PMID:Staccato left anterior descending artery occlusion: a recognizable subset of unstable angina. 387 32

Calcium antagonists have become accepted agents for the attenuation of myocardial ischemia when it becomes manifest as angina pectoris. However, it is not known whether these agents can protect ischemic myocardium during the early evolution of an acute myocardial infarct. Calcium antagonists could potentially improve myocardial perfusion, by relieving coronary spasm or improving collateral blood flow, and reduce the energy demands of the ischemic myocardium either directly or by reducing heart rate or contractility. In some studies, calcium antagonists have decreased the rate of adenosine triphosphate depletion in ischemia and reduced functional or structural indexes of ischemic injury after relatively brief periods (up to 2 hours) of injury. We have assessed the ability of verapamil to protect severely ischemic myocardium in dogs with a 40-minute test period of circumflex occlusion followed by reperfusion. After 4 days of recovery, infarcts were sized by histologic methods. Untreated dogs had subendocardial infarcts (the more moderately ischemic subepicardial region being salvaged by reperfusion). Pretreatment with verapamil reduced the size of these subendocardial infarcts from 34 +/- 8 to 8 +/- 3% of the ischemic circumflex vascular bed (anatomic area at risk). Thus, verapamil prevented cell death in a substantial proportion of the severely ischemic subendocardial region that otherwise would have died as a result of the 40-minute test period of ischemia. To establish whether verapamil could prevent cell death for a longer period of time in the less severely ischemic subepicardial region, a 3-hour period of coronary occlusion with reperfusion was studied.
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PMID:Effects of calcium-channel blockers on myocardial preservation during experimental acute myocardial infarction. 388 3

A case of a patient with variant angina associated with severe ventricular tachyarrhythmias studied by continuous electrocardiographic and haemodynamic monitoring is reported. Severe ventricular arrhythmias developed both during maximal ST-segment elevation, in association with haemodynamic signs of acute ischaemic cardiac dysfunction and after nitroglycerin-induced reversion of ischaemia and return of the haemodynamic variables to the basal state. Thus, in this patient, ventricular arrhythmias during acute ischaemia could be related not only to acute vasospastic coronary occlusion but probably also to reperfusion after relief of coronary spasm.
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PMID:Occlusion and reperfusion as possible different mechanisms of ventricular tachyarrhythmias in Prinzmetal's variant angina. 393 46

Acute increases in left ventricular (LV) diastolic pressure relative to volume occur during angina in humans and after pacing tachycardia in dogs with coronary stenoses. In this study we assessed myocardial function following pacing tachycardia in dogs with coronary stenoses and compared it with function of the same myocardial segment during coronary occlusion. Also we calculated regional wall stiffness following pacing tachycardia in dogs with coronary stenoses. In anesthetized dogs with two-vessel critical (90%) coronary stenoses, ultrasonic crystals were implanted subendocardially to measure either anterior wall (AW) and lateral wall (LW) segment lengths (SL; n = 14) or LV wall thickness (h; n = 7). LV pressure was measured using a high-fidelity micromanometer catheter. After pacing tachycardia in dogs with two-vessel coronary stenoses, there was a substantial rise in LV end-diastolic pressure (from 6 +/- 1 to 15 +/- 1 mmHg; P less than 0.001), a slight increase in end-diastolic segment length (AWEDSL from 15.6 +/- 1.0 to 16.4 +/- 1.0 mm; p less than 0.01; and LWEDSL from 13.8 +/- 1.4 to 14.3 +/- 1.4 mm; P greater than 0.01) and a reduction of percent systolic shortening of the ischemic segments. An upward shift of the diastolic pressure-SL relation was observed in the postpacing period. During coronary occlusion the diastolic pressure-SL relation of the same segment shifted rightward, or rightward and downward, and systolic shortening became holosystolic bulging. Ischemia due to coronary stenoses plus increased O2 demand had substantially different effects on regional wall motion and segmental diastolic mechanics than did ischemia due to coronary occlusion. Over the same range of residual transmural LV diastolic pressure, the radial stiffness modulus was higher after pacing tachycardia in the presence of coronary stenoses.
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PMID:Different effects of two types of ischemia on myocardial systolic and diastolic function. 399 9

The effects of nicardipine, a phenyldihydropyridine calcium-channel antagonist agent, have been investigated on regional blood flow and epicardial ST-segment elevation in the nonischemic and ischemic myocardial zones after either intermittent, or permanent coronary artery occlusion in dogs. Whichever the experimental model used, nicardipine reduced heart rate and arterial blood pressure and increased regional myocardial blood flows (50 to 100% of control flow values). All these effects were dose-dependent. During intermittent coronary occlusion (a model that mimics angina pectoris), the nicardipine-induced myocardial vasodilation was homogeneous between the endocardium and the epicardium of the ischemic and nonischemic zones. During permanent coronary occlusion (a model that mimics myocardial infarction), the nicardipine-induced myocardial vasodilation mainly developed within the endocardium of the ischemic zone, leading thus to a beneficial transmural blood flow redistribution in that zone. Finally, and whichever the experimental model used, nicardipine did not reduce the ischemic injury as assessed by epicardial ST-segment elevation.
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PMID:[Effects of nicardipine on regional coronary deficit and the ST segment of the healthy and ischemic myocardium in dogs]. 399 52

This study was designed to determine whether human hearts release adenosine, a possible regulator of coronary flow, during temporary myocardial ischemia and, if so, to examine the mechanisms involved. Release of adenosine from canine hearts had been reported during reactive hyperemia following brief coronary occlusion, and we initially confirmed this observation in six dogs hearts. Angina was then produced in 15 patients with anginal syndrome and severe coronary atherosclerosis by rapid atrial pacing during diagnostic studies. In 13 of these patients, adenosine appeared in coronary sinus blood, at a mean level of 40 nmol/100 ml blood (SE = +/-9). In 11 of these 13, adenosine was not detectable in control or recovery samples; when measured, there was concomitant production of lactate and minimal leakage of K(+), but no significant release of creatine phosphokinase, lactic acid dehydrogenase, creatine, or Na(+). THERE WAS NO DETECTABLE RELEASE OF ADENOSINE BY HEARTS DURING PACING OR EXERCISE IN THREE CONTROL GROUPS OF PATIENTS: nine with anginal syndrome and severe coronary atherosclerosis who did not develop angina or produce lactate during rapid pacing, five with normal coronaries and no myocardial disease, and three with normal coronaries but with left ventricular failure. The results indicate that human hearts release significant amounts of adenosine during severe regional myocardial ischemia and anaerobic metabolism. Adenosine release might provide a useful supplementary index of the early effects of ischemia on myocardial metabolism, and might influence regional coronary flow during or after angina pectoris.
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PMID:Release of adenosine from human hearts during angina induced by rapid atrial pacing. 482 35

Spasm is only one type of dynamic stenosis typically responsible for variant angina; spasm with or without transient intraluminal plugging, superimposed on a wide range of old or fresh, fixed stenoses, is largely responsible for unstable angina; physiological changes of tone around pliable coronary stenoses probably account for the variable exercise tolerance and for spontaneous attacks in patients with stable angina. Sustained spasms, not responsive to nitrates and thrombosis, are likely to be involved at different times or simultaneously in acute coronary occlusion causing myocardial infarction. Acute or worsening phases of coronary diseases are largely caused by dynamic stenoses, whereas stable, fixed-threshold, predictable angina may be the only feature of quiescent phases of coronary disease.
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PMID:Spasm and dynamic coronary stenoses. 608 11

The complications reported in the first 1500 patients enrolled in the National Heart, Lung, and Blood Institute Percutaneous Transluminal Coronary Angioplasty (PTCA) Registry are analyzed. Data were contributed from 73 centers between September 1977 and April 1981. PTCA was successful in 63% of attempts. Five hundred forty-three in-hospital complications occurred in 314 patients (21%). The most frequent complications were prolonged angina in 121, myocardial infarction (MI) in 72, and coronary occlusion in 70. One hundred thirty-eight patients (9.2%) had major complications (MI, emergency surgery or in-hospital death). One hundred two patients (6.8%) required emergency surgery, usually for coronary dissection or coronary occlusion. Sixteen patients (1.1%) died in-hospital; the mortality rate was 0.85% in patients with one-vessel disease and 1.9% in those with multivessel disease. The mortality rate was significantly higher in patients who had had bypass surgery (p less than 0.001). Nonfatal complications were significantly influenced by the presence of unstable angina (p less than 0.001) and initial lesion severity greater than 90% diameter stenosis (p less than 0.001). This report delineates and assesses the complications encountered with PTCA during its initial 3 1/2-year clinical experience. These results support the relative safety of PTCA as a method of nonsurgical myocardial revascularization in carefully selected patients.
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PMID:Percutaneous transluminal coronary angioplasty: report of complications from the National Heart, Lung, and Blood Institute PTCA Registry. 621 38


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