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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Within a relatively short period of time, nitroglycerin patches have come into widespread use for treatment of coronary artery disease in the absence of sufficient clinical data in support of their efficacy. Presently, there is still considerable controversy regarding the extent and duration of action as well as the dosage requirements. Accordingly, a study was carried out in six patients with angiographically-documented coronary artery disease, stable exercise-induced angina pectoris and reproducible ST-segment depression to analyze the effects of nitroglycerin patches, formulated to deliver 5 mg, 10 mg, 20 mg as well as 30 mg per 24 hours, respectively, on the extent of ST-segment depression. In a further study, the extent and duration of antianginal and anti-ischemic effects of nitroglycerin patches delivering 30 mg/24 hours were investigated in ten patients according to a randomized, double-blind, crossover placebo-controlled protocol. In seven of these patients, testing was again performed at 2.5 hours after repeated application (second application at 24 hours) (Figure 1). Nitroglycerin patches delivering 5 mg, 10 mg, 20 mg as well as 30 mg/24 hours, respectively, led to significant reductions in ST-segment depression at 2.5 hours of 59% (range 25 to 100%; p less than 0.025), 63% (0 to 100%, p less than 0.01), 77% (50 to 100%, p less than 0.001) as well as 82% (50 to 100%, p less than 0.005) as compared with control values (Figure 2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[High-dose transdermal nitroglycerin therapy: loss of effect within 24 hours?]. 392 12

Nitroglycerin 0.5 mg sublingually was tested in two exercise protocols in order to determine the time of onset of the anti-anginal action. When patients stopped exertion after nitroglycerin administered at the time of moderate chest pain and one minute before stopping exercise, no anti-anginal or anti-ischaemic effect was seen compared with a placebo-medicated test given double-blindly. When the patients continued exertion after nitroglycerin administered at the onset of chest pain, a significant decrease in chest pain intensity and an improvement in ST-segment depression was seen. It is concluded that administration of a quick-acting anti-anginal drug at the onset of chest pain during continued bicycle exercise provides a suitable test model to determine the time of onset of action in exertional angina pectoris.
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PMID:The time of onset of action of sublingual nitroglycerin in exercise-induced angina pectoris. A methodological study. 393 Feb 48

The effects of both intracoronary and intravenous administration of nitroglycerin on transmural distribution of blood flow in the left ventricle after partial coronary artery occlusion was investigated using two independent methods. In 16 open chest, anesthetized dogs, tubing supplying the cannulated left coronary artery was partially occluded. Strain gauges sutured paralled to superficial and deep fibers of the myocardium separately recorded the contractile force of each layer. With occlusion set so that depression of the deep contractile force was imminent. 12 mug intracoronary nitroglycerin in seven dogs depressed only the deep contractile force without changing systemic hemodynamics. Intravenous administration of 180 mug nitroglycerin in nine dogs resulted in a decrease of deep contractile force and aortic pressure often associated with an increase in superficial contractile force. Distribution of myocardial blood flow during peak coronary flow after intracoronary administration of nitroglycerin or during a decrease in aortic pressure after intravenous nitroglycerin administration was determined by the tissue uptake of an intracoronary bolus of rubidium-(80). This was compared with the uptake of potassium-(42) injected before nitroglycerin. Intravenous or intracoronary administration of nitroglycerin caused a significant reduction in subendocardial blood flow with a decrease in the subendocardial/subepicardial ratio of isotope. These experiments suggest that under conditions of acute partial coronary occlusion, the autoregulatory response results in more fully dilated subendocardial vessels causing them to be less responsive to nitroglycerin. Nitroglycerin may then reduce the vascular resistance in the subepicardial more than the subendocardial vessels, resulting in a "steal" of blood flow from deep to superficial myocardium.
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PMID:Nitroglycerin and heterogeneity of myocardial blood flow. Reduced subendocardial blood flow and ventricular contractile force. 463 92

Antianginal efficacy and improved exercise performance with timolol, a new beta-adrenergic blocking agent, was assessed in 23 patients with chronic stable angina pectoris in an 11-week double-blind, placebo-controlled study. Twenty-two of the 23 subjects completed the open-label phase of this investigation (weeks 0 to 6) while receiving 10 to 30 mg of timolol twice daily to optimize exercise capacity. Weekly anginal episodes and nitroglycerin consumption declined from 8.9 +/- 9.1 episodes/week and 8.1 +/- 10.6 tablets/week, respectively, with placebo to 2.7 +/- 5.2 episodes/week and 2.6 +/- 6.0 tablets/week with optimal timolol dose (p less than 0.05). Resting heart rate (HR) and systolic blood pressure (SBP) also decreased from 75.2 +/- 14.0 beats/min and 139.1 +/- 15.7 mm Hg with placebo to 55.1 +/- 8.9 beats/min and 130.5 +/- 15.9 mm Hg with timolol (p less than 0.05). Peak exercise HR, peak exercise SBP, and peak exercise double product (HR X SBP) were significantly (p less than 0.05) reduced when evaluated 12 to 13 hours after administration of timolol compared with placebo (101.5 +/- 21.1 beats/min verus 193.3 +/- 96.2 beats/min, 161.5 +/- 26.7 mm Hg versus 175.6 + 20.8 mm Hg, and 16.6 +/- 5.1 X 10(-3) versus 21.7 +/- 5.4 X 10(-3), respectively). Exercise duration was prolonged from 263.3 +/- 90.2 seconds to 330.3 +/- 73.9 seconds (p less than 0.05), while time to onset of 1 mm S-T segment depression was delayed in 15 patients from 231.8 +/- 86.4 seconds to 298.7 +/- 68.4 seconds (p less than 0.05). During the double-blind phase (weeks 7 to 10), 8 subjects received timolol and 11 patients received placebo. Nitroglycerin consumption at weeks 8 and 10 and anginal frequency at week 8 were unchanged compared with initial placebo treatment. Resting HR, peak exercise HR, and peak exercise double product were significantly attenuated at weeks 8 and 10 in timolol patients compared with their initial placebo exposure. However, these variables were unchanged in placebo subjects compared with their initial placebo therapy. Exercise duration was again prolonged at week 8 in timolol subjects compared with initial placebo results (315.1 +/- 61.2 seconds versus 261.3 +/- 68.8 seconds, p less than 0.05), but not at week 10. Placebo patients demonstrated no difference at week 8 or 10 in exercise performance compared with initial placebo treatment. Timolol twice daily, therefore, is potentially useful in some patients with angina pectoris. Other patients may, however, require a shorter dose interval for optimal angina control and maximal improvement in exercise capacity.
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PMID:Antianginal efficacy and improved exercise performance with timolol. Twice-daily beta blockade in ischemic heart disease. 612 94

Right ventricular angiography was performed in 46 patients with acquired valvular heart disease and 8 normal subjects. Right ventricular ejection fraction (RVEF) correlated highly only with right ventricular peak systolic pressure (RVPSP) and mean pulmonary artery pressure, both in patients with and without tricuspid insufficiency. For the group, RVEF = -0.33 RVPSP + 63 (correlation coefficient [r] = -0.76, probability [p] less than 0.001). Of 20 patients with moderate or severe elevation of pulmonary artery pressure, 17 (85%) had an abnormally low ejection fraction (less than 47%), while 19 (73%) of 26 patients with normal or mildly elevated pulmonary artery pressure had a normal right ventricular ejection fraction. In seven patients with elevated pulmonary artery pressure, a second ventriculogram was performed during intravenous nitroglycerin administration. Nitroglycerin produced a significant decrease in right ventricular peak systolic pressure (59 +/- 22 to 49 +/- 18 mm Hg, mean +/- standard deviation) (p less than 0.05) and in end-systolic volume (71 +/- 16 to 59 +/- 11 m1/m2) (p less than 0.05), and an increase in ejection fraction (43 +/- 9 to 48 +/- 7%) (p less than 0.05). Thus, at least part of the depression of ejection fraction in patients with elevated pulmonary pressure is reversible with a decrease in pulmonary artery pressure.
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PMID:Right ventricular function in valvular heart disease: relation to pulmonary artery pressure. 640 52

The influence of indomethacin therapy on the circulatory and antianginal effects of nitroglycerin were studied in six patients with stable angina pectoris. Indomethacin 50 mg or identical placebo capsules were administered three times a day for 1 week each in a double-blind, random manner. Heart rate, blood pressure, and ST-segment depression were measured at rest and during exercise before and after the administration of 0.6 mg sublingual nitroglycerin during indomethacin and placebo therapy. Nitroglycerin lowered standing systolic blood pressure by 38 mm Hg during placebo therapy (p less than 0.001) and by 36 mm Hg during indomethacin therapy (p less than 0.001). This was accompanied by a reflex increase in heart rate (p less than 0.001) which was of similar magnitude during placebo and indomethacin therapy. The increase in exercise duration to the onset of angina post nitroglycerin was similar during placebo and indomethacin therapy (128 vs 84 s; NS). Similarly, the increase in the total duration of exercise post nitroglycerin was similar during placebo and indomethacin therapy. Reduction in ST-segment depression post nitroglycerin was more pronounced during placebo than indomethacin therapy, but did not achieve statistical significance. The results show that indomethacin did not modify the circulatory effects of nitroglycerin at rest or during exercise and did not attenuate the increase in exercise tolerance produced by sublingual nitroglycerin. Since indomethacin is a potent prostaglandin inhibitor, the findings indirectly suggest that the vasodepressor and antianginal effects of nitroglycerin are in all probability not mediated by prostaglandins.
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PMID:Interaction of indomethacin and nitroglycerin on hemodynamics and exercise tolerance in patients with angina pectoris. 642 Oct 13

A series of 12 consecutive patients with Prinzmetal's variant angina is presented. There was a preponderance of males (eight/12) and individuals less than 60 years of age (nine/12). Delay in diagnosis was frequent, primarily due to difficulty in achieving a proper 12 lead ECG recording of the attack which often occurred late at night or in the early morning, subsiding within minutes. In some cases, moreover, ST-depression was observed in the ECG monitoring lead as a reciprocal manifestation of subepicardial ischaemia or due to incorrect polarity in the monitoring lead. The incidence of serious arrhythmias, AV-block and ventricular tachycardia was high (eight/12); two patients had to be DC-converted. Coronary arteriography revealed a spectrum from normal or nearly normal coronary arteries to single vessel disease. Nitroglycerin was well suited for treatment of acute attacks. Long-term treatment with calcium antagonists was effective and without serious side-effects. The follow-up time was from 8 months to 5 years (mean 2 years). It is concluded that Prinzmetal's variant angina as such is a rare disease, but that coronary artery spasm is most likely an important contributory factor in the clinical manifestations of coronary artery disease: arrhythmias, sudden death and myocardial infarction.
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PMID:Prinzmetal's variant angina. 678 40

Nadolol, a new nonselective beta 1 and beta 2 adrenergic blocking agent, has a plasma half-life of 17 to 23 hours. We studied 37 volunteers with stable angina pectoris who had five or more episodes of pain per week and who also had a 1 mm or greater ST segment depression 80 msec past the J point during a Bruce protocol treadmill test. An eight-week placebo controlled run-in period preceded double-blind randomization to nadolol administered once per day (17 patients) or identical appearing placebo for four weeks (20 patients), after which an exercise test was done. Diaries for pain episodes and nitroglycerin consumption were kept. Exercise tests were performed 24 hours after the last nadolol or placebo dose. Episodes of pain per week were reduced 59.8 percent after nadolol and 28.2 percent after placebo (P less than .01). Nitroglycerin consumption after nadolol was reduced 66.8 percent while after placebo it was reduced 36.2 percent (P less than .05). Resting and peak heart rates and peak rate-pressure products showed typical reductions due to beta-blockade 24 hours after nadolol compared with stability of these during placebo, all P less than .001. Exercise time after nadolol increased 42.2 percent, which was more than the 14.5 percent increase after placebo (P less than .05). Exercise work after nadolol increased 64.7 percent, greater than the 22 percent increase after placebo (P less than .05). Mean ST segment depression at end of exercise was little changed before and after treatment in both groups, reflecting consistency of effort. Improvement in symptoms and work capacity associated with nadolol significantly exceeded the placebo group responses. Unlike other available agents of this class, a single daily dose of nadolol produced therapeutically effective 24-hour beta-blockade in patients with disabling angina pectoris.
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PMID:Comparison of nadolol, a new long-acting beta-receptor blocking agent, and placebo in the treatment of stable angina pectoris. 679 83

In 20 infarct patients, whose age varies from 43 to 78 years (m 59.6), continuous hemodynamic measurements were made to determine the cardiovascular effects of propranolol without and during a simultaneous infusion treatment with nitroglycerin. In cases of compensated ventricular function and pulmonary wedged pressures of 15 mm Hg or less (N = 10), a mean intravenous propranolol dose of 6.1 +/- 1.3 mg led to a significant reduction of the LVSWI and a simultaneous increase of the PCP by 31% of the control value (P less than or equal to 0.005). A simultaneously performed infusion treatment with nitroglycerin at a mean dose of 3.0 +/- 1.6 mg/h resulted in totally cutting off the propranolol-induced PCP increase, whereas a decrease of the heart rate and the LVSWI due to a beta-receptor-blockade remained completely unchanged. In the case of pre-existing congestion insufficiency of the left ventricle (N = 10) and of a pulmonary wedged pressure of above 15 mm Hg, the administration of a mean dose of propranolol of 5.8 +/- 1.1 mg for protection of the myocardium resulted in a partly disquieting decrease of the volume of cardiac output (P less than or equal to 0.005) which was 28% of the control value for the CI an 12% for the SVI. Correspondingly the left ventricular stroke work decreased to 18%. Nitroglycerin has a reducing influence on these changes, but not down to the initial level. In cases of sufficient ventricular function, propranolol has a favorable influence on the myocardial O2-metabolism via its depressor effect on heart rate and contractility. By means of nitroglycerin, an increase of the pulmonary wedged pressure occurring under this condition can be inhibited. However, in the case of a pre-existing congestion insufficiency, propranolol can lead to a partly disquieting depression of the circulation, which, apart from the hemodynamic risks, makes a rather unfavorable influence on the myocardial O2-metabolism seem likely.
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PMID:[The treatment of acute myocardial infarctions with beta-receptor-blockers. II. Hemodynamic effects of propranolol with and without combination therapy with nitroglycerin (author's transl)]. 679 41

It is known that intravenous administration of dipyridamole can induce chest pain and ECG signs of ischemia in patients with coronary artery disease. In the present study we evaluated ECG and hemodynamic changes in response to dipyridamole (0.56 mg/kg in 10 min) under basal conditions and 3 hours after administration of nitroglycerin (10 mg/24 h patch) in 14 patients with coronary artery disease. The effects of nitroglycerin were also compared to those induced by the same drug on a bicycle stress test in the same patients. Exercise stress test induced specific ST changes in all patients when performed off-drug. Nitroglycerin administration completely prevented exercise-induced ischemia in 2 patients, and significantly prolonged exercise time in the remaining patients (p < 0.01). This effect was accompanied by a significant increase in heart rate (HR) and rate-pressure product at the threshold of ischemia (HRBP, p < 0.01); furthermore we observed a significant increase in HR at the maximal work load (p < 0.05). In the absence of treatment, dipyridamole infusion induced ST segment changes and/or typical chest pain in 12/14 patients. Moreover we observed a significant increase (p < 0.05) in HR, BP and HRBP during the test with respect to basal conditions. Following nitroglycerin administration, dipyridamole infusion failed to induce ischemia in 4 patients, and the time to ST depression in the remaining 8 patients (459 +/- 69 vs 610 +/- 127 s; p < 0.05) was significantly prolonged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[ECG-dipyridamole and ECG-exercise test in the assessment of ischemic cardiopathy: effects of the acute administration of nitroglycerin]. 755 92


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