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)

Nisoldipine is a new calcium channel blocker of the dihydropyridine family with a high affinity for coronary vessels. We assessed the efficacy of nisoldipine in the treatment of asymptomatic ischemia in 12 patients with chronic, stable angina. Two to four weeks of daily therapy with prn nitroglycerin and placebo was followed by 24-hour ambulatory electrocardiographic recording for ST segment assessment. After two weeks of once-daily nisoldipine, 10 to 20 mg, the ambulatory recording was repeated. A significant difference was seen in ischemia-magnitude products of asymptomatic ischemic episodes in placebo versus active drug periods (P less than .05). When total ischemic burden was considered (ST segment depression during both painless and painful episodes), the difference was even more significant (P less than .02).
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PMID:Silent myocardial ischemia: improvement with nisoldipine therapy. 264 67

A placebo-controlled, double-blind, crossover study was conducted to determine the effects of nifedipine (60 to 90 mg per day) monotherapy and propranolol (240 mg per day) monotherapy on symptoms, angina threshold, and cardiac function in patients with chronic stable angina. Following a two-week placebo period, patients were randomly assigned to receive either nifedipine or propranolol for a five-week treatment period, after which they crossed over to the alternative regimen. All 21 patients were men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. New York Heart Association functional class improved in patients taking either nifedipine or propranolol, and nitroglycerin consumption decreased with both treatments compared with placebo. Nifedipine significantly delayed the onset of chest pain and 1 mm of ST-segment depression during bicycle exercise; increases with propranolol were smaller and not statistically significant. Nine patients had a preferential clinical response to nifedipine compared with six patients to propranolol; this was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvement in radionuclide ejection fraction at identical work loads. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14 percent (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output. Thus, nifedipine is more effective on several measurements than propranolol when administered as single drug therapy in stable angina and has the advantage of preserving cardiac output during exercise.
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PMID:Chronic stable angina monotherapy. Nifedipine versus propranolol. 264 28

In patients with recurrent chest pain in the immediate postinfarction state, one must determine whether the recurrent chest discomfort is related to myocardial ischemia or not. If recurrent ischemia is present then it may be due to either (1) transient increase of myocardial oxygen demand over a fixed coronary reserve, (2) transient decrease of myocardial oxygen supply, or (3) a combination of both. Coronary angiography reveals that most patients have double or triple vessel disease. The presence of postinfarction angina portends a poor prognosis. Reinfarction rate has been reported as high as 28% during initial hospitalization and mortality has been as high as 57% at six months follow-up. Intravenous nitroglycerin seems to be an important foundation therapy for the management of postinfarction angina. The use of beta blockers has reduced mortality by 24% compared to placebo in this patient subgroup. Calcium antagonists have proven efficacious in patients with non-Q-wave myocardial infarction and postinfarction angina. Thrombolytic therapy, chronic anticoagulation and antiplatelet therapy are not proven efficacious at this time. Coronary angioplasty is usually successful initially but is associated with an early myocardial infarction rate varying from 1.4 to 13%. Mortality rate is usually low as is late myocardial infarction rate. Recurrent angina occurs commonly in these patients. Surgical therapy in the early infarction state should be offered to those patients who have a poor response to maximal medical therapy whose coronary artery obstructions are not amenable to PTCA. At the time of coronary angiography if partially occlusive thrombus is identified, intravenous heparin and aspirin should be given to prevent more thrombus formation and total occlusion.
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PMID:Early postinfarction angina: therapeutic strategies. 269 Nov 42

Vascular responses to many physiological stresses are abnormal in heart failure. Increased peripheral resistance and a reduction in the vasodilator response to exercise and ischemia are examples of this abnormal vascular control. Such abnormal vascular control in heart failure is a result of interplay between neural, hormonal, and local vascular factors. This study was designed to test the hypothesis that a specific local mechanism, endothelium-dependent relaxation to acetylcholine (ACh), is depressed in experimental heart failure. Experiments were performed on 11 purebred beagles. Experimental heart failure was induced by rapid ventricular pacing for approximately 30 days. Femoral artery diameter was measured by sonomicrometry, and dose-response relationships to ACh, norepinephrine (NE), and nitroglycerin (NTG) were done before and after inhibition of cyclooxygenase by indomethacin. Heart failure resulted in a significant depression of ACh relaxation at all concentrations. In dogs with heart failure, indomethacin enhanced the dilation response to low concentrations of ACh. Constriction to NE and dilation to NTG were unchanged by heart failure. These data demonstrate that in the canine femoral artery endothelium-dependent dilation to ACh is depressed in experimental heart failure. Depression of endothelium-dependent vasodilation represents one local mechanism for abnormal control of the vasculature in congestive heart failure.
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PMID:Heart failure depresses endothelium-dependent responses in canine femoral artery. 270 66

A reduced coronary flow reserve has been reported in patients with ischemia-like symptoms and normal coronary arteries. In 13 such subjects both coronary vasomotion and flow reserve were studied. The luminal area of the proximal and distal third of the left anterior descending and left circumflex artery were determined by biplane quantitative coronary arteriography using a computer-assisted system. Subjects were studied at rest, during submaximal supine bicycle exercise (4.0 min, 116 W) and 5 min after sublingual administration of 1.6 mg nitroglycerin. Heart rate, mean pulmonary and aortic pressure as well as the percent change of both proximal and distal luminal area were determined. In 10 of the 13 subjects, coronary sinus blood flow was measured by coronary sinus thermodilution technique at rest and after dipyridamole infusion (0.5 mg/Kg in 15 min) 10 +/- 5 days after quantitative coronary arteriography. Coronary flow ratio (dipyridamole/rest) and coronary resistance ratio (rest/dipyridamole) were determined in these subjects. Subjects were divided into 2 groups according to the behaviour of the coronary vessels during exercise (vasodilation = Group 1, vasoconstriction = Group 2). Coronary vasodilation of the proximal (luminal area + 26%; p less than 0.001) and distal (+ 45%; p less than 0.001) artery was observed in 7 subjects (Group 1) during exercise and after sublingual nitroglycerin (+46%; p less than 0.001 and +99%; p less than 0.001, respectively). In Group 2 (n = 6), however, there was coronary vasoconstriction of the distal vessel segments (-24%; p less than 0.001) during exercise, whereas the proximal coronary artery showed vasodilation (+ 26%; p less than 0.001) during exercise. Following sublingual nitroglycerin, both vessel segments elicited vasodilation (distal coronary + 44%; p less than 0.001, proximal coronary artery +47%; p less than 0.001). Coronary flow ratio amounted to 2.5 in Group 1 and to 1.2 in Group 2 (p less than 0.05) and coronary resistance ratio to 2.7 in Group 1 and to 1.2 in Group 2 (p less than 0.05), respectively. Thus, among subjects with ischemia-like symptoms and normal coronary arteries there is a subgroup of patients (Group 2) with an abnormal dilator response of the distal coronary arteries to the physiologic dilator stimulus of exercise and a reduced dilator capacity of the resistance vessels after dipyridamole (= abnormal coronary vasodilator syndrome). The nature of this exercise-induced distal coronary vasoconstriction is not clear but might be due to an abnormal neurohumoral tone which may cause or contribute to the blunted vascular response during exercise.
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PMID:[Abnormal coronary vasomotility in subjects with normal coronary arteries and reduced reserve of coronary flow]. 272 Jul 12

The long-term course of angina and the electrocardiographic signs of ischemia were assessed in 13 patients (10 women and 3 men, mean age 49 +/- 6 years) with typical angina pectoris, positive exercise tests, no evidence of coronary spasm and angiographically normal coronary arteries (syndrome X). Clinical and electrocardiographic parameters as well as results of exercise testing and 24-hour electrocardiographic monitoring were assessed at presentation and after a mean follow-up of 6.3 years (range 3 to 9). Mean number of anginal episodes and nitroglycerin consumption per week were similar at presentation and at the last follow-up. Furthermore, no significant difference was noted in heart rate-systolic blood pressure product at 0.1 mV of ST-segment depression (20,363 +/- 5,747 vs 21,649 +/- 5,687 beats/min x mm Hg), at angina (19,223 +/- 5,680 vs 20,126 +/- 6,023 beats/min x mm Hg) and at peak exercise (22,057 +/- 5,669 vs 22,868 +/- 6,122 beats/min x mm Hg). Time to 0.1 mV of ST-segment depression, to angina and to peak exercise was also similar (595 +/- 163 vs 631 +/- 184 s, 524 +/- 156 vs 571 +/- 168 s and 671 +/- 168 vs 718 +/- 186 s, respectively). The number of episodes of ST-segment depression greater than or equal to 0.1 mV during electrocardiographic monitoring was similar at presentation and follow-up (31 vs 25) as was the proportion of painful episodes (39 vs 36%). None of the patients developed major coronary events or cardiomyopathy during follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term variability of angina pectoris and electrocardiographic signs of ischemia in syndrome X. 274 23

Thirteen patients, seven with acute myocardial infarction and six survivors of sudden death after sport, underwent coronary angiography within a mean of 104 min after the onset of symptoms. The admission electrocardiogram showed transmural myocardial ischemia in all patients. The ischemia-related vessel was occluded in all cases of sudden death and in three cases of acute myocardial infarction. Reperfusion was achieved in eight vessels: after intracoronary streptokinase in three, after intracoronary nitroglycerin in three, and mechanically in two. Coronary spasm was demonstrated in three vessels, and coronary thrombi, in four. The coronary lesion was described as either concentric in two or eccentric with irregular borders in eight. There was a high incidence of eccentric lesions consistent with ruptured plaques. The acute coronary angiographic findings of acute myocardial infarction and sudden death after sport are similar. Physical exercise can provoke myocardial infarction and sudden death probably by inducing plaque rupture that can evoke coronary spasm, thrombosis, or both.
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PMID:Myocardial infarction and sudden death after sport: acute coronary angiographic findings. 276 51

A 77-year-old woman with suspected coronary artery disease underwent an oral dipyridamole/thallium-201 myocardial imaging study. Approximately 75 minutes after ingestion of dipyridamole 300 mg suspension, the patient developed chest pain, hypotension, nausea, and diaphoresis. An electrocardiogram revealed ST-T wave changes suggestive of inferior ischemia. Appropriate therapeutic measures, including aminophylline and nitroglycerin, were instituted. Delayed thallium images revealed reversible ischemia in the anteroseptal and posterobasal regions with a fixed defect in the inferobasal region. Cardiac enzyme studies were also indicative of acute myocardial injury. The patient subsequently underwent coronary arteriography and four-vessel coronary artery bypass grafting and was discharged without further complication. This report raises concerns about the potential danger of dipyridamole in patients with severe coronary artery stenosis and collateral circulation. Prophylactic aminophylline should be considered in these patients.
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PMID:Myocardial infarction after dipyridamole-assisted thallium-201 imaging. 280 May 78

Twenty patients on chronic beta-blockade for angina pectoris were included in a double-blind randomized cross-over placebo-controlled study on a 2% nitroglycerin gel administered transdermally by an adhesive. Topinitro. The dose, 2.5-10 mg/day, was individually titrated and each treatment period was 28 days. The effect was evaluated by exercise tests and diary cards for anginal attacks and nitroglycerin tablets consumed. Results. In the 17 patients who completed the trial, active treatment did not influence systolic and diastolic blood pressure or resting and maximal heart rate. Maximal performance increased insignificantly from 92 +/- 23 to 96 +/- 20 W. The level at which 1 mm of ST depression appeared increased from 62 +/- 26 to 73 +/- 28 W (p less than 0.05). The number of attacks decreased significantly, from 92 +/- 30 to 14 +/- 28/4 weeks. The reduction in the number of sublingual nitroglycerin tablets consumed was insignificant. Conclusion. Nitroglycerin adhesive, in individual dosages, may improve signs and symptoms of ischemia.
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PMID:Effects on angina pectoris and exercise tests of a 2% nitroglycerin gel adhesive in patients on chronic beta-blockade. A placebo-controlled study. 287 Jun 10

Investigations into the mechanisms and characteristics of ischemic heart disease have increasingly documented evidence of myocardial ischemia in the absence of symptoms. Recent work using objective criteria of ischemic episodes confirmed that angina pectoris or its equivalents need not accompany myocardial ischemia and noted that these episodes appear to be quite common. The impact on prognosis awaits further study, but preliminary data suggest an adverse prognosis for patients with recurrent spontaneous silent vasoconstrictive ischemia. Furthermore, treatment of silent ischemic episodes with nitrates may be associated with reduced ischemia. Preliminary trials show reduction of the number, duration, and magnitude of silent ischemic episodes by transdermal nitroglycerin given to patients receiving beta-blockers. Therapy of acute ischemic syndromes should be designed to eliminate ischemia completely, not merely ameliorate pain.
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PMID:Treatment of silent myocardial ischemia with transdermal nitroglycerin added to beta-blockers and alprazolam. 287 35


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