Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with stable coronary artery disease commonly have transient myocardial ischemia with or without experiencing angina, but the prognostic implications of this "total ischemic burden" is still a matter of debate. We studied 112 consecutive patients with coronary artery disease, normal left ventricular function at rest and exercise-induced myocardial ischemia, a 24-hour ambulatory EKG was performed after drug withdrawal. The mean exercise duration was 572 +/- 192 seconds, with an ischemic threshold (ST depression = 1 mm) of 390 +/- 190 seconds). By Holter monitoring 30 patients had no ischemia and 82 (73%) had a total of 332 episodes of ST segment changes, the majority of which were asymptomatic (242/332, 73%). Among 82 patients with transient myocardial ischemia, 44 (54%) had only asymptomatic episodes. Nine patients (11%) complained of angina coincident to ST changes. Twenty-nine patients (35%) had both painful and painless ST segment alterations. All patients were prospectively followed-up while on conventional medical therapy. During a mean follow up of 25 +/- 10 months cardiac events occurred in 31 patients; there were 5 cardiac deaths, 3 non-fatal myocardial infarctions, 2 hospitalization for unstable angina and 21 revascularization procedures (PTCA or CABG). By multivariate analysis the number of stenotic vessels on coronary angiography was predictive of the events during the follow-up (p = 0.03), while other demographic, clinical, ergometric and angiographic variables were not influential. Event-free survival was similar for all subsets of transient myocardial ischemia (silent, symptomatic, or none).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prognostic value of total ischemic burden in patients with stable ischemic heart disease. 176 34

"Painless" or silent myocardial ischemia is common and may be associated with all types of coronary insufficiency. Repeated ischemia impairs the functional and anatomical status of the ventricle and the aim of the treatment of coronary insufficiency must be to reduce not only pain, when present, but also ischemia. A distinction must be drawn between: 1) Painless ischemia after myocardial infarction occurring in a high risk group. This requires investigation of the patient, medical treatment and, according to results, angioplasty or surgery. 2) Painless ischemia associated with stable or unstable angina. It is known that in stable angina 50 per cent of ischemia attacks are painless and that complete treatment must seek to reduce the duration of ischemia. Treatment is adjusted on the basis of the results of investigations and the severity of ischemia. 3) Silent ischemia alone which requires precise diagnostic evaluation and assessment of risk based upon the patient's condition.
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PMID:[Silent ischemia. Therapeutic strategy]. 178 31

Ca antagonists of the dihydropyridine class (DHPs) are a heterogeneous group of drugs that interfere with Ca entry into vascular smooth muscle cells of resistance arterioles through type-L calcium channels producing arteriolar vasodilation. This leads to a reduction of vascular tone and, therefore, they have been successfully used in the treatment of systemic hypertension, myocardial ischemia (stable, variant, and unstable angina and silent ischemia), and Raynaud's phenomenon. Furthermore, recent clinical trials have indicated that DHPs may induce regression or slowing the progression of atheroma in coronary arteries. The results obtained with DHPs in the prophylaxis of migraine headache and in treating ischemic stroke and cerebral artery vasospasm are encouraging. However, more carefully designed, double-blind, large-scale, long-term studies are needed to better define the therapeutic value of DHPs in these disorders, the severity of adverse effects, and the mechanism responsible for their therapeutic effects.
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PMID:Dihydropyridines and vascular diseases. 179 15

Results of our prospective, randomised pilot trial to evaluate the clinical effects and the angiographic correlates of early thrombolysis in patients with unstable angina are reported. Sixty-seven patients had coronary angiography 10 +/- 8 (median 7) hours after an episode of transient chest pain at rest with reversible ischaemic changes on the electrocardiogram. Patients with left main disease (4), or diffuse coronary disease and unidentified ischemia-producing lesions (13) were excluded, as were those without severe (greater than or equal to 70%) stenosis (10). Intracoronary thrombus was identified at angiography in 7 patients (17%) and complex coronary lesions in 5 (12%) of the remaining 40 patients who were randomised to either intracoronary streptokinase 250,000 IU followed by intravenous heparin along with conventional treatment (20 patients), or to conventional treatment alone (20 patients). All patients received Aspirin. No differences between the streptokinase and the conventional treatment groups were observed with respect to demographic and clinical characteristics at admission to the study. During observation in the intensive care unit for 3 +/- 1 days, 8 patients (40%) with streptokinase and 10 (50%) with conventional treatment were free from angina and infarction (p = 0.75; 95% confidence interval for the difference in response rates = -20 to 40%). There were no bleeding complications and no patient died. Patients enrolled in our study had fewer coronary thrombi at angiography than currently reported. Our data did not show that adjunct treatment with streptokinase and heparin is superior to conventional treatment alone in these patients.
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PMID:Intracoronary streptokinase in unstable angina: a prospective randomised study. 180 19

Frequency and duration of silent myocardial ischemia (SMI) on Holter recording were determined in 20 patients with unstable angina before and after 4 weeks of intensive triple drug therapy with oral nitrates (20-80 mg daily), betablocker (metoprolol 100-200 mg/day) and calcium channel blocker (nifedipine 40-80 mg/day). The number of ischemic episodes decreased from 445 (409 silent) to 149 (140 silent) (p less than 0.001), and mean duration of silent and symptomatic ischemia per patient decreased from 5.9 +/- 3.3 minutes to 2.4 +/- 2.6 minutes (p less than 0.001) and 4.1 +/- 5.5 minutes to 1.4 +/- 2.8 minutes (p less than 0.001) respectively. Intensive medical therapy is effective in ameliorating SMI in patients with unstable angina.
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PMID:Frequency and duration of silent myocardial ischemia in patients with unstable angina before and after intensive medical therapy. 182 Oct 1

This investigation was designed to determine if acute ischemic cardiac injury causes the release of the 98 amino acid (aa) N-terminus of the 126 aa atrial natriuretic factor prohormone (pro ANF). Seventeen patients with acute myocardial infarction, but without clinical evidence of congestive heart failure, had their circulating concentrations of the whole N-terminus (ie, pro ANF 1-98), the midportion of the N-terminus of the ANF prohormone (consisting of aa 31-67; pro ANF 31-67) and creatine phosphokinase (CPK) monitored daily for 14 days. All seventeen patients had elevated plasma pro ANF 1-98 and pro ANF 31-67 concentrations at the time of presentation. Maximal increase on day three post-infarction correlated with the size of infarction estimated by the maximal CPK (r = 0.675; p less than 0.05) but did not correlate with the amount of left ventricular dysfunction. Another three patients with acute myocardial infarction were treated with tissue plasminogen activator (tPA). The measured pro ANF 1-98 and pro ANF 31-67 levels in these patients were within our normal range and significantly lower (p less than 0.001) than seen in patients with acute myocardial infarction not given thrombolytic therapy. Six patients with unstable angina, likewise, had normal circulating pro ANFs 1-98 and 31-67 concentrations during prolonged episodes of chest pain. These data suggest that myocardial necrosis but not ischemia triggers the release of the entire 126 aa prohormone.
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PMID:Acute and sustained release of the atrial natriuretic factor prohormone N-terminus with acute myocardial infarction. 182 42

Clinical features of 37 cases of stunned myocardium were studied. Mean duration of asynergy was 22.6 +/- 15.7 days. In all 11 cases of unstable angina without any significant serum creatine kinase leakage, the duration of asynergy was within 14 days. Related coronary lesions were reperfused (spontaneously or by interventional therapy) to TIMI grade II or higher. Transient Q waves were observed in 39% of all cases. Negative T waves tended to be prolonged, and persisted after disappearance of asynergy in 74% of all cases. 201Tl uptake in the stunned area varied widely between individual cases (ranging from "absent" to "normal"), although it became normal in all cases in the chronic stage. Mal-distribution of 99mTc-pyrophosphate (PYP) to the endocardial side of the stunned area was observed in 33%. In 186 cases of acute coronary syndrome, we studied whether or not reversibility of ischemia-disturbed myocardium could be predicted by simultaneous dual isotope SPECT, and found that 201Tl-uptake in the chronic stage significantly improved in the region showing absence of 99mTc-PYP accumulation or maldistribution of 99mTc-PYP to the endocardial side, while reversibility of the region showing transmural 99mTc-PYP accumulation and a dought pattern was poor. Ischemia-associated myocardial damage recovered to various degrees, and dual isotope SPECT was useful in evaluating the reversibility of such damage already at the acute stage.
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PMID:Clinical study of the stunned myocardium. 183 73

Acute myocardial ischemia results from an increased cardiac workload in presence of a critical coronary stenosis (demand ischemia), coronary occlusion (supply ischemia) or a combination of both. It is complicated by cardiac arrhythmias and deterioration of function of ischemic myocardium and results in an increased load and dilatation of non-ischemic myocardium. Cardiac protection in acute myocardial ischemia can be related to preservation of coronary blood flow, function of ischemic and non-ischemic myocardium or prevention of cardiac arrhythmias. In control animals and humans, ACE-inhibitors have no major effect on coronary blood flow. Myocardial ischemia raises plasma-renin-activity, angiotensin I-conversion by passage through coronary circulation, and plasma-angiotensin-II-concentrations. ACE-inhibitors and angiotensin-II-receptor blockers increase coronary blood flow during myocardial ischemia. Other mechanisms (bradykinin potentiation) may be involved. We found a potentiation of the coronary dilatory effect of the neuropeptide neurotensin (which is probably mediated by prostaglandins) by ACE-inhibitor. ACE-inhibitor may delay infarct development in animal experiments and improve function of ischemic myocardium. The importance of early dilatation of non-ischemic myocardium is unknown and it is unclear whether it may be prevented by an ACE-inhibitor as was shown for late dilatation. Studies on the effect of ACE-inhibitors in exercise-induced angina pectoris are controversial. An antiischemic and coronary dilatory effect has been shown by invasive studies in patients. A preliminary study in unstable angina pectoris was positive. Beneficial hemodynamic and antiarrhythmic effects (as well as excessive hypotension, however) have been shown in patients with acute myocardial infarction.
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PMID:[Possibilities of ACE inhibitor therapy in acute myocardial ischemia]. 186 31

Variants of unstable angina pectoris were compared upon examination of 366 relevant patients. 24-h ECG monitoring registered painless ST shifts in 75 of them. Treatment at hospital produced results independent of ischemia form (painful or painless). However, the analysis of long-term response for 10 patients demonstrating episodes of ischemia at discharge suggests that in spite of numerous adjustments of treatment in 70% of the patients the risk of unfavorable outcome seems great.
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PMID:[Unstable stenocardia: prognostic significance of painless forms of myocardial ischemia during hospitalization and in the remote period]. 186 49

After successful thrombolytic treatment for acute myocardial infarction, recurrent ischemia and infarction may occur with little warning. Coronary lesion morphology was analyzed from angiograms performed in 72 consecutive patients at 1 to 8 days after streptokinase treatment for acute myocardial infarction and the data were evaluated in relation to the subsequent clinical course. All patients were clinically stable at the time of angiography and continued to receive heparin infusion for greater than or equal to 4 days after thrombolysis. The infarct-related artery was patent in 55 patients (76%). In the 10 days after angiography, 15 patients developed prolonged episodes of angina at rest; the condition of 4 stabilized with medical treatment, but 11 required urgent medical intervention (coronary angioplasty in 8 and bypass surgery in 3). There were no differences in age, gender, left ventricular function or extent of coronary artery disease between those patients who developed unstable angina and those who had a stable in-hospital course. However, the median plaque ulceration index of the infarct-related lesion was 6.7 (95% confidence limits 6.3, 10) in the 15 patients with an unstable course versus 3.3 (2, 4.4) in those with a stable course (p less than 0.001). There were no differences between the two patient groups in the severity of stenosis, length of diseased segment, symmetry/eccentricity, presence of a shoulder, location at branch point or bend, presence of globular or linear filling defects, contrast staining or collateral supply. These data show that after thrombolysis, the degree of irregularity of the infarct-related artery is a critical determinant of early clinical instability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Irregular coronary lesion morphology after thrombolysis predicts early clinical instability. 186 30


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