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

In a randomized double-blind, placebo-controlled, crossover trial, the potential anti-ischaemic action of the angiotensin-converting enzyme (ACE) inhibitor spirapril was studied in 19 patients with coronary artery disease (CAD) and reproducible exercise-induced ST-segment depression, but without hypertension or congestive heart failure. Measurements of blood pressure and heart rate as well as exercise-testing were performed after 2 weeks of treatment each with placebo and spirapril. Anginal attacks and consumption of short-acting nitrates were recorded in the patients' diaries. Resting blood pressure was not significantly reduced (143 +/- 20/89 +/- 10 mmHg vs 138 +/- 17/87 +/- 10 mmHg). The exercise-induced ST-segment depression, the main criterion for anti-ischaemic effect, was 2.17 +/- 1.72 mm after placebo and not significantly affected by spirapril (2.03 +/- 1.47 mm) despite a significant reduction in blood pressure x heart rate product at maximum workload (213 +/- 45.4 vs 197.5 +/- 36.8; p < 0.05). The number of anginal attacks per week and nitrate consumption remained virtually unchanged. A significant reduction of exercise-induced ischaemia in normotensive patients with CAD was not demonstrated with spirapril.
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PMID:Angiotensin-converting enzyme inhibition with spirapril in patients with coronary artery disease. 806 51

The diagnostic usefulness of dipyridamole-stress two-dimensional echocardiography was assessed in 82 patients consisting of 27 patients with angina pectoris, 42 with myocardial infarction, and 13 control subjects. Two-dimensional echocardiographic monitoring was performed during dipyridamole infusion: 0.56 mg/kg for 4 minutes, then discontinuation for 4 minutes, followed by a final infusion of 0.28 mg/kg for 2 minutes. The cumulative dose was 0.84 mg/kg. Worsening or fixed wall motion abnormality with unaffected baseline indicated a positive finding. All patients underwent coronary angiography. The sensitivity and specificity of dipyridamole-stress two-dimensional echocardiography for diagnosis of significant coronary artery stenosis (> or = 75%) were 84% (58/69) and 92% (12/13), respectively. The sensitivity of this method for the branches of the coronary artery was 85% for the left anterior descending artery, 80% for the right coronary artery, and 75% for the left circumflex artery. The sensitivity for single-, double-, triple-vessel disease was 75%, 81% and 100%, respectively. The sensitivity and specificity of the dipyridamole electrocardiogram (ST depression more than 0.1 mV) were 33% (23/69) and 77% (10/13), respectively. The appearance of dipyridamole-stress induced wall motion abnormality was significantly earlier than those of chest pain and ST segment depression. Side effects were observed in 43% (35/82) of patients, but were only mild and transient. Dipyridamole-stress two-dimensional echocardiography is the best method for detecting coronary artery stenosis and predicting the localization of lesion sites.
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PMID:[Diagnosis of ischemic heart disease by dipyridamole-stress two-dimensional echocardiography]. 815 34

This study evaluates dipyridamole stress echocardiography in silent ischemia. Fourteen patients with previous coronary artery bypass grafting (group A) and 16 patients with healed myocardial infarction (group B) were studied. All had > or = 1 mm ST depression without chest pain during bicycle exercise testing. Left ventricular wall motion was analyzed using a computerized display of digital systolic cineloops with a high frame rate. Test results were compared with coronary angiography. Dipyridamole echocardiography accurately identified patients with significant coronary artery stenosis in both groups (3 of 4 in group A, 11 of 14 in group B). Retrograde flow to the occluded native artery was associated with positive results on dipyridamole testing in 6 of 7 patients in group A and all 3 in group B. Sensitivity, specificity and diagnostic accuracy for detecting significant coronary stenosis or occlusions with retrograde flow was 78, 100 and 83%, respectively. Patients with angiographic multivessel disease had a significantly larger increase in wall motion score index during dipyridamole stress than patients with 0- or 1-vessel disease, 0.18 +/- 0.11 versus 0.05 +/- 0.18 (p < 0.05). Two patients developed symptomatic bradycardia and hypotension during dipyridamole infusion. It is concluded that dipyridamole echocardiography accurately identifies myocardial regions with restricted coronary flow. Stress echocardiography is a valuable tool for assessing coronary flow in silent ischemia.
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PMID:Digital dipyridamole stress echocardiography in silent ischemia after coronary artery bypass grafting and/or after healing of acute myocardial infarction. 824 37

Twenty-five normotensive patients with stable angina, angiographically documented coronary disease and normal left ventricular function were randomized to a crossover study comparing atenolol 100 mg x 1, sustained-release diltiazem 120 mg x 2, and their combination. A maximal symptom limited bicycle exercise test and a 24-h ambulatory electrocardiographic (ECG) monitoring were performed at the end of each treatment period. Exercise duration was increased equally in the different treatment groups. Time to onset of 1-mm ST-segment depression was longer with atenolol (P < 0.02) and combination therapy (P < 0.01) than with diltiazem. The maximal ST-segment depression was decreased with atenolol (P < 0.05) and combination therapy (P < 0.02), whereas, time to onset of angina was prolonged only with combination therapy (P < 0.03). The number of ischaemic episodes during ambulatory monitoring was lower with atenolol and combination therapy than with diltiazem (P < 0.01). The difference between atenolol and diltiazem was mainly due to lower ischaemic activity with atenolol between 06:00 h and 12:00 h (P < 0.05). Anginal frequency (P < 0.01) and nitroglycerin consumption (P < 0.05) were lower with combination therapy than with monotherapy. Thus, while comparable effects were achieved on clinical variables, atenolol appeared to be more effective than diltiazem, reducing myocardial ischaemia during exercise and ambulatory monitoring. With combination therapy, both clinical and electrocardiograph signs of ischaemia were improved.
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PMID:Effects of atenolol and diltiazem on exercise tolerance and ambulatory ischaemia. 834 77

Changes in electrocardiogram R-wave amplitude are often noted during treadmill stress testing. The two main reasons for this phenomenon discussed in the literature are left ventricular dimension changes and myocardial ischemia. To evaluate the relation between myocardial ischemia and electrocardiogram R-wave amplitude changes, we investigated in a retrospective study the data of 99 patients (20 females/79 males) with clinical signs of coronary artery disease. All patients had undergone exercise ECG and dipyridamole test. Electrocardiogram R-wave amplitude changes and ST-segment alterations were measured before, during and after provocation by bicycle stress test and intravenous dipyridamole. In neither test was there a specific reaction of R-wave amplitude to myocardial ischemia. During myocardial ischemia there were patients with an increase as well as a decrease R-wave amplitude. There was no significant correlation between the reaction of the R-wave amplitude in the exercise ECG when compared with the Dipyridamole test. Quantitative analysis showed a reduction of R-wave amplitude during maximum provocation in both tests, which was statistically significant in almost every subgroup of patients. In both tests the ST-segment depression was statistically significant in all groups, but there was no significant correlation between the reaction of R-wave amplitude and the ST-segment depression. In conclusion, there is no specific reaction of R-wave amplitude to myocardial ischemia. It is very unlikely, that the often noted changes in R-wave amplitude during stress testing are caused by ischemic episodes of the myocardium. Other mechanisms must be sought to explain the observed R-wave alterations.
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PMID:[Is there a specific response of the ECG R-wave amplitude to exercise-induced myocardial ischemia? Exercise test and dipyridamole test]. 845 60

The usefulness of high-dose (< or = 0.84 mg/kg over 10 minutes) dipyridamole echocardiography testing was compared with that of exercise thallium-201 scintigraphy in detecting restenosis (> 70% lumen reduction) in 50 asymptomatic patients with ST-segment depression during maximal exercise testing 3 months after successful coronary angioplasty. Dipyridamole echocardiography testing and exercise thallium scintigraphy showed a similar sensitivity (75 vs 83%; p = NS) and specificity (90 vs 84%; p = NS) for the detection of restenoses, which occurred in 12 patients. It is concluded that dipyridamole echocardiography testing is as accurate as exercise thallium testing for the noninvasive detection of severe restenosis in patients with exercise-induced asymptomatic ST-segment depression after successful angioplasty. Furthermore, the site, extent and severity of the thallium perfusion defects during exercise are correlated to those of the dyssynergy during dipyridamole echocardiography.
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PMID:Exercise thallium scintigraphy versus high-dose dipyridamole echocardiography testing for detection of asymptomatic restenosis in patients with positive exercise tests after coronary angioplasty. 847 68

1. Using an extracellular recording technique, we have investigated the site of action of adenosine and muscarine on the rat superior cervical ganglion (SCG). The adenosine-induced hyperpolarization and muscarine-induced depolarization of ganglia were localized to the cell bodies of the ganglia. Responses to muscarine and adenosine were larger when recorded via the internal carotid nerve (ICN) compared with the external carotid nerve. Depression of the response to muscarine by adenosine was similar for both nerve trunks. 2. The effects of adenosine and cyclic nucleotides on the d.c. potential and the depolarization to muscarine were examined by recording via the ICN. Adenosine at concentrations up to 1 mM produced concentration-dependent hyperpolarizations. Hyperpolarization induced by 100 microM adenosine was unaffected by 1 microM tetrodotoxin or the muscarinic M1-receptor antagonist pirenzepine (0.3 microM). In contrast, hyperpolarizations to 100 microM adenosine were significantly reduced by 10 microM 8-phenytheophylline (55 +/- 7 microV vs 15 +/- 9 microV, P < 0.01, n = 4). Two agents known to increase intracellular cAMP, i.e. 8-bromo-cyclic-adenosine-3'-5' monophosphate (8BrcAMP) and isoprenaline, depolarized ganglia. Depolarizations to 100 nM mucarine were significantly depressed by adenosine (100 microM) by 26 +/- 2% (n = 61), but unaltered by 8BrcAMP or cyclic guanosine-3'-5' monophosphate. 3. Dipyridamole and hydroxy-nitro-benzylthioguanosine (inhibitors of adenosine transport) and erythro-6-amino-9-(2-hydroxy-3-nonyl)adenine (EHNA, an inhibitor of adenosine deaminase), potentiated the depression by adenosine of the response to muscarine, and the hyperpolarization to adenosine respectively. However, there was no evidence to support the hypothesis that there was spontaneous release of endogenous adenosine under the conditions of study, as dipyridamole or EHNA did not alter the control d.c. potential or the depolarization to muscarine. 4. It is concluded that the ability of adenosine to hyperpolarize and depress the response of the rat SCG to muscarine is due to the direct activation of postsynaptic somatodendritic P1-purinoceptors and unlikely to be mediated by an increase in intracellular cAMP. In addition the rat SCG has mechanisms for both the uptake and inactivation of adenosine.
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PMID:On the site of action and inactivation of adenosine by the rat superior cervical ganglion. 851 24

Cardiac L-carnitine content, essential for mitochondrial fatty acid transport and ATP-ADP exchange, decreases during ischemia. In animal models, administration of the natural derivative, L-propionylcarnitine, may reduce ischemia and improve cardiac function. To evaluate possible antiischemic effects of L-propionylcarnitine was compared with placebo in a randomized, double-blind, parallel design, in addition to preexisting therapy. Patients with > or = 2 anginal attacks per week and objective signs of ischemia with angina during bicycle exercise testing were included. After an initial 2-week, single-blind placebo phase, 37 patients received 500 mg L-propionylcarnitine tid, and 37 patients received placebo for 6 weeks. Both groups were comparable at baseline. Three patients discontinued the study while on placebo (two because of noncompliance, one because of palpitations) and one while on L-propionylcarnitine (noncompliance). Although heart rate, blood pressure at rest, and maximal exercise were not affected, L-propionylcarnitine increased the time to 0.1 mV ST-segment depression [44 +/- 3 vs. 8 +/- 2 seconds (mean +/- SEM) in the placebo group; p = 0.05], and exercise duration improved by 5% compared with placebo. Anginal attacks and the consumption of nitroglycerin were not affected in either group. Thus, following a 6 week treatment period, L-propionylcarnitine induced additional, albeit marginal, antiischemic effects in anginal patients who were still symptomatic despite maximal conventional antianginal therapy. It is questionable whether in these patients this form of metabolic treatment will achieve great benefit, although in some improvement can be expected.
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PMID:Additional antiischemic effects of long-term L-propionylcarnitine in anginal patients treated with conventional antianginal therapy. 885 Mar 78

The purpose of the present study is to assess the effect of nicorandil, a coronary vasodilator with a mechanism of potassium channel opening, on the abnormal myocardial 201Tl perfusion evoked by exercise. Eleven patients who had a history of typical angina, positive exercise electrocardiograms, positive 201Tl scintigraphy, nearly normal coronary arteriograms, and negative coronary vasospasm underwent exercise 201Tl scintigraphies under no medication (baseline test) and administration of nicorandil (nicorandil test). 201Tl was injected at a matched workload in both tests. Nicorandil did not alter heart rate, blood pressure, or the rate-pressure product at the end of the exercise, but it significantly improved the extent score from 0.37 +/- 0.22 to 0.20 +/- 0.15 (p < 0.05) and the severity score from 33.9 +/- 32.2 to 13.5 +/- 16.4 (p < 0.05), and also significantly hastened the 201Tl mean washout rate from 30.5 +/- 14.8% to 37.4 +/- 13.1% (p < 0.05). Anginal symptoms disappeared in 3 of 5 cases and ST depression improved in 5 of 7 cases after nicorandil. We conclude that nicorandil augments coronary flow reserve, possibly due to a reduction of vasotone in the small coronary arteries.
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PMID:Effect of nicorandil on abnormal coronary flow reserve assessed by exercise 201Tl scintigraphy in patients with angina pectoris and nearly normal coronary arteriograms. 885 Mar 79

Intravenous dipyridamole induces angina pectoris (AP) in some patients with significant coronary artery disease (CAD). The aim of this prospective study was to identify the angiographic, nuclear, and clinical determinants. The authors examined 50 patients consecutively with significant CAD on coronary angiography. All antiischemic medications were stopped twenty-four hours (nitrates only 6 hours) before injection of dipyridamole (0.84 mg/kg). ECGs were taken before, during, and after this injection. The regional myocardial activity of Tc-99m-Sestamibi at rest and after dipyridamole injection was measured with single-photon emission computed tomography (SPECT). During dipyridamole injection 20 patients had AP, of whom 15 had ST segment depression on ECG (P < 0.001). The only significant difference on coronary angiography between patients with dipyridamole-induced AP and those without AP was the presence of collaterals (P < 0.05). In patients with AP and collaterals, ECG and SPECT changes were always noted in the collateralized territory. Subgroup analysis showed that patients without previous myocardial infarction (MI, n = 17, P < 0.05) or nontransmural MI (n = 17, P < 0.05) had a good correlation between collaterals and AP, whereas patients with a history of transmural MI (n = 16) did not. No further significant variables could be found as a predictor of AP after dipyridamole injection. These findings suggest that AP during dipyridamole stress test is due to ischemia, which is not related to the severity of CAD. Ischemia is probably due to coronary steal to the collateralized territory in patients without transmural MI. Dipyridamole-induced angina pectoris is predictive for collaterals and may indicate viability in patients with MI.
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PMID:Dipyridamole-induced angina pectoris during sestamibi stress test in patients with significant coronary artery disease: clinical, angiographic, and nuclear determinants. 911 78


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