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)

Diltiazem, a calcium channel blocking agent, has potent cardiovascular effects that are directly related to its influence on vascular smooth muscle, ventricular myocardium, and specialized conducting tissue. It causes coronary and peripheral vasodilation, has a negative chronotropic and dromotropic effect, and little to no negative inotropic effect in patients with normal ventricular function. Diltiazem has potential use in a wide variety of cardiovascular disorders. It has been shown extremely effective in relieving the coronary artery spasm associated with variant angina. When compared with nitrates in patients with exertional angina, diltiazem has similar efficacy. Preliminary work indicates it will have a therapeutic role in the treatment of unstable angina. Because of its ability to improve the balance between myocardial oxygen supply and demand and reduce cellular injury secondary to ischemia, it is likely that diltiazem will be of benefit in the treatment of acutely ischemic myocardium during cardiopulmonary bypass and possibly acute myocardial infarction. It has proven efficacy in treating re-entrant supraventricular tachycardia. Adverse effects are seen in less than 5% of patients, indicating that it is well tolerated.
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PMID:The use of diltiazem hydrochloride in cardiovascular disorders. 676 99

The clinical manifestations of symptomatic coronary arterial spasm were analyzed in 30 patients whose coronary arteriograms demonstrated no fixed severe obstructions. The study group consisted of 14 men and 16 women (average age, 47 years). Angina at rest was invariable and it was usually typical in quality, location, duration and response to nitroglycerin. Exertional angina occurred in 23 percent and syncope with angina in 33 percent. Spontaneous remission of angina for at least 1 month occurred in 57 percent of patients. Prinzmetal's variant angina occurred in 77 percent of patients and only S-T segment depression or T wave changes during angina occurred in 23 percent. Major arrhythmias during ischemia developed in 47 percent. Exericse tests were positive in 24 percent. Myocardial infarction, probably due to coronary spasm, occurred in 7 percent of patients. Isosorbide dinitrate and propranolol were effective therapy in only 39 percent and 6 percent of patients, respectively. Nifedipine, a calcium flux antagonist, was effective in 80 percent of patients. Patients with normal coronary arteriograms who have clinical features suggestive of coronary arterial spasm should be considered for further investigation, including long-term electrocardiographic monitoring and provocative testing for spasm.
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PMID:Syndrome of symptomatic coronary arterial spasm with nearly normal coronary arteriograms. 698 57

The efficacy of nifedipine in relieving recurrent ischemic episodes following acute myocardial infarction was studied in 11 patients a mean of 9.2 days post infarction (range 2-42 days). Prior to infarction, all of the patients had a history of exertional angina only, yet following the infarction, episodes of recurrent ischemia occurred at rest in spite of maximal medical management with beta-blockers and/or nitrate preparations, which lowered the heart rate to a mean of 65 beats/min, and the blood pressure to a mean of 109/70 mmHg. Ischemic episodes were associated with ST-segment elevation in 7 patients and ST-segment depression or T-wave inversion in 4 patients. Coronary angiography was performed in 8 patients, and demonstrated multivessel coronary disease in 7. The episodes of rest ischemia were prevented in all but one patient by the addition of nifedipine (mean daily dose 60 mg, range 40-120 mg) without causing a change in heart rate or blood pressure. Two patients continued to have myocardial ischemia with minimal exertion, although rest pains were abolished, and they underwent coronary bypass surgery for relief of exertional pain. Only one patient continued to have episodes of ischemia at rest, although the frequency of ischemic episodes was decreased, and bypass surgery was necessary for pain relief. The other 8 patients have been managed medically for a mean of 5.4 months (range 1-12 months) and have remained pain free on combined regimens of nifedipine, beta blockers, and/or nitrate preparations. We conclude that nifedipine may be efficacious for the relief of recurrent myocardial ischemia at rest following acute infarction. In some patients nifedipine may eliminate the need for coronary artery bypass surgery and in others it may provide clinical stability prior to operation.
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PMID:Nifedipine therapy for recurrent ischemic pain following myocardial infarction. 708 48

To determine if patients with rest angina have more severe regional ischemia than patients with exertional angina, we compared the severity of left coronary artery (LCA) stenosis in 29 patients with transient anterior ischemic ST-T changes at rest, and 30 patients with anterior ST changes only during exertion. The percentage diameter stenosis was measured with Vernier calipers as (2 x lesion diameter x 100 percent)/(prestenotic + poststenotic diameter). There was no difference between the two groups in the mean diameter stenosis of unoccluded LCA vessels either when all vessels were compared (rest: 69 +/- 12 percent; exertional: 70 +/- 13 percent [p = NS]) or when only the maximal stenosis in each patient was compared (rest: 74 +/- 10 percent; exertional: 75 +/- 12 percent [p = NS]). Total occlusion of at least one major vessel of the LCA also occurred with similar frequency in patients with rest (6/29) and exertional (12/30) angina (p = NS). However, collateral development distal to 76-100 percent LCA lesions was significantly less frequent in rest angina (4/21 vessels [19 percent]) than in exertional angina (21/30 vessels [70 percent]), (p less than .03). We conclude that patients with rest angina do not have more severe coronary stenosis than patients with exertional angina, but frequently may have more severe regional ischemia due to reduced collaterization of jeopardized myocardium.
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PMID:Regional coronary anatomy in rest angina. Comparison of patients with rest and exertional angina using quantitative coronary angiography. 711 59

The role of systemic arterial hypertension as a possible trigger of myocardial ischemia during angina at rest was studied in 13 consecutive patients who also had a history of exertional angina. Significant (greater than or equal to 70%) stenosis of at least one major vessel was present in each of the 10 patients in whom coronary arteriography was carried out. After documentation of the electrocardiographic and arterial blood pressure changes during two or more episodes of resting angina, i.v. methoxamine was infused under continuous monitoring of the ECG, arterial blood pressure and pulmonary artery diastolic pressure. The heart rate was maintained either spontaneously or by atrial pacing to levels similar to those during angina at rest. Despite increases in arterial blood pressure and the double product (systolic blood pressure x heart rate) to levels higher than those during spontaneous angina in all patients, no chest pain or electrocardiographic changes occurred in nine patients. In the other four patients, however, angina supervened. Three of these four patients, but only one of the remaining nine, had a borderline or elevated pulmonary artery diastolic pressure at rest. We conclude that in a considerable number of patients with "nonvariant" resting angina, acute increases in arterial blood pressure during the spontaneous attacks are not likely to be the cause of myocardial ischemia. Nevertheless, in some of these patients, increases in resting pulmonary artery diastolic pressure may favor the development of ischemia during afterload augmentation.
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PMID:Acute arterial hypertension during spontaneous angina in patients with fixed coronary stenosis and exertional angina: an associated rather than a triggering phenomenon. 723 26

This report describes a case of a patient with a history of classical angina of effort which developed into an unstable progressive syndrome. A 42-year-old-woman was admitted to the hospital because of resting angina pectoris. Examination revealed signs of septal subepicardial ischemia in the resting electrocardiogram and a positive ergometric test with marked depression of the S-T segment. Hemodynamic studies showed in the ventriculogram a clearly defined area of hypokinesis on the anterolateral segment of the ventricle and the coronariography revealed normal vessels. During exercise the patient developed anginal pain and an elevation of the S-T segment in a lead II electrocardiogram. During the pain episode, selective left and right coronariographies showed the presence of a severe spasm in the first portion of the anterior descending branch. In the course of one of the injections the patient developed ventricular fibrillation, this was reverted with a 400 watts/sec shock. The patient was discharged from the hospital a few days after and has been successfully treated with nitrates and calcium blocking agents. This case represents the first time that a coronary spasm in normal vessels has been adequately documented by us.
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PMID:[Exercise-induced coronary artery spasm. Angiographic demonstration and results of medical treatment]. 732 47

A new circulatory system, "physiologic anteroperfusion system", has been developed and tested in 6 patients with significant proximal coronary artery stenosis. Prolonged and safe balloon inflation was possible without any ischemic signs. The system consists of an electronic cardiac synchroperfusor which, by activating a pulsatile unit, permits increased diastolic anteroperfusion of autologous blood under physiologic pressure through low-profile standard angioplasty catheters. This study reports the results obtained in 6 patients during proximal prolonged percutaneous transluminal coronary angioplasty. Four men and two women suffering from severe exertional angina pectoris, with normal resting left ventricular function, no collaterals and excellent apical two-dimensional four-chamber echocardiographic views were studied. After a 90 +/- 10 seconds of control occlusion under continuous monitoring of hemodynamics, electrocardiograms (3 to 4 leads), two-dimensional echo and chest pain grading, a second balloon inflation protected by the physiologic anteroperfusion system at a flow rate of 44 +/- 12 ml/min was performed for fifteen minutes. The ischemic signs present in the myocardium depending on the occluded artery were totally abolished during prolonged inflation protected by physiologic anteroperfusion system. All the patients were successfully dilated and were discharged from hospital the following morning without cardiac enzyme elevation or signs of central or peripheral hemolysis. Conclusion, in 6 patients with severe proximal coronary artery stenosis, safe prolonged proximal angioplasty without signs of ischemia was performed using a new simple physiologic anteroperfusion system, which allows active diastolic flow-pressure controlled autologous arterial blood perfusion, through standard low profile catheters.
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PMID:[Synchronized anterograde perfusion during percutaneous transluminal coronary angioplasty: preliminary clinical study]. 748 91

The causes of hypertensive microvascular ischemia are reviewed along with diagnostic factors. Stress/rest thallium-201 scintigraphy is shown to have a predictive value of 78% for a diagnosis of microvascular disease in hypertensive patients with exertional angina and left ventricular hypertrophy. Lack of isotope uptake at peak stress correlates well with the decrease in coronary flow reserve in ischemic segments, which is 2-3 times lower than in normal subjects. Treatment with enalapril produces regression of left ventricular hypertrophy, normalization of thallium-201 uptake, and an increase in exercise capacity in patients with microvascular angina.
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PMID:Microvascular angina in systemic hypertension: diagnosis and treatment with enalapril. 749 15

This study describes the results of Dobutamine stress echocardiography in 10 patients with Syndrome X. The diagnosis of Syndrome X was made on the basis of the presence of exertional angina, positive exercise stress test, negative ergonovine stress test and normal coronary arteries at angiography. All patients underwent Dobutamine stress echocardiography after interruption of any antianginal therapy. Dobutamine was infused starting with a dose of 5 mcg/kg/min over 3 minutes with incremental steps of 5 mcg/kg/min every 3 minutes up to a maximal dose of 40 mcg/kg/min. Two-dimensional echocardiography and 12-lead electrocardiography was monitored during the infusion of the drug. Nine patients received the maximal dose while one patient prematurely stopped the test for the occurrence of side effects. None of the ten patients developed segmental left ventricular wall motion abnormalities indicative of myocardial ischemia; ST-segment depression diagnostic for ischemia developed in 30% of patients; angina was elicited in one of these patients and in two additional patients. A hyperkinetic response to Dobutamine infusion involving all the segments of the left ventricle was observed both in patients with and without chest pain or electrocardiographic changes. In patients with Syndrome X Dobutamine induces a hyperkinetic left ventricular response indicative of normal contractile reserve despite the presence in some cases of angina and electrocardiographic signs of ischemia.
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PMID:Results of dobutamine stress echocardiography in patients with syndrome X. 796 53

The purpose of this study was to investigate the effects of beraprost sodium, a stable prostacyclin analog, on the parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina. Thirty-one patients with exertional angina who had significant organic coronary artery stenosis in at least one of the three major coronary arteries were selected. All patients underwent quantitative exercise thallium-201 emission computed tomography before and 1 month after 120 micrograms per day of beraprost sodium administration. Before exercise, blood samples were collected from 8:30 a.m. to 9:30 a.m. after the patients had been lying in bed undisturbed for at least 10 minutes. Plasma platelet factor 4 (PF4), fibrinopeptide A (FPA), tissue plasminogen activator antigen (t-PA), and plasminogen activator inhibitor-1 activity (PAI-1) were measured. There were no significant differences in exercise parameters on both exercise tests. However, both the extent and severity scores of ischemia were significantly aggravated (p < 0.05 for both) during beraprost sodium administration. Plasma FPA levels decreased significantly during beraprost sodium administration (p < 0.01). Likewise, plasma PF4 levels decreased significantly during beraprost sodium administration (p < 0.05). As for plasma t-PA antigen levels, there was no significant difference before versus during beraprost sodium administration. Plasma PAI-1 activity levels decreased significantly during beraprost sodium administration (p < 0.05). The results indicate that beraprost sodium has strong antithrombogenic properties. However, its aggravation of myocardial ischemia may limit clinical usage.
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PMID:Effects of beraprost sodium, a new prostaglandin I2 analog, on parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina. 854 11


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