Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is uncertain whether dobutamine echocardiography is a better test than exercise electrocardiography for the detection of coronary disease in patients who can exercise. We compared the hemodynamics, sensitivity, and specificity of these tests in 24 patients, 16 with coronary disease and 8 controls. The tests were performed within six weeks of one another and were interpreted without knowledge of other clinical data. The exercise electrocardiogram was considered abnormal if the patient developed one mm of ST-segment depression, while the dobutamine test (up to 40 micrograms/kg/min) was considered abnormal if the patient developed ST-segment depression or a left ventricular wall motion abnormality. Exercise testing resulted in a higher heart rate (145 +/- 29 vs. 110 +/- 24, p less than 0.001) and blood pressure (176 +/- 31 vs. 148 +/- 24, p less than 0.001). Dobutamine testing was 25% more sensitive than exercise testing (94 vs. 69%, 95% confidence interval for difference is 0 to 50%, p = 0.09), while exercise testing was 38% more specific (88 vs. 50%, 95% confidence interval for difference is -3 to 79%, p = 0.14). We conclude that exercise results in a higher heart rate and blood pressure than dobutamine infusion. Differences in sensitivity and specificity are inconclusive, but indicate that the sensitivity of exercise testing is, at best, equivalent to dobutamine testing, while any increase in specificity with dobutamine testing, compared with exercise testing, would not be clinically significant.
Clin Cardiol 1992 Sep
PMID:Comparison of exercise electrocardiography and dobutamine echocardiography. 139 98

Myoglobin is known to protect the mechanical function of the heart from hypoxia by acting as a sarcoplasmic oxygen reservoir and shuttle. We postulated a role for myoglobin in the pathogenesis of congestive heart failure. Several models of congestive heart failure were employed to test the hypothesis, including spontaneous inherited dilated cardiomyopathy in Doberman Pinschers, and heart failure produced by rapid ventricular pacing in dogs, volume overload in chickens and furazolidone toxicity in turkeys. Myocardial myoglobin was decreased by approximately 50% for all models (P less than 0.05). In Doberman Pinschers dogs which are predisposed to the development of dilated cardiomyopathy and have mild subclinical depression of cardiac performance, myocardial myoglobin (1.05 +/- 0.22 mg/g) is approximately 50% decreased compared to healthy mongrel dogs (2.15 +/- 0.52 mg/g), approximately twice as much as dobermans with heart failure (0.47 +/- 0.25 mg/g) but similar to the concentration found in dogs paced to heart failure (1.09 +/- 0.34 mg/g). Myocardium from poultry had remarkably decreased myoglobin compared to mammals (34 +/- 4 micrograms/g) with heart failure produced either by furazolidone or salt toxicity causing a further 50% reduction. In the canine models of heart failure, myocardial myoglobin concentration was demonstrated to be correlated with biochemical and physiological indicators of myocardial performance, namely, mitochondrial and sarcoplasmic reticular ATPase activities, and cardiac output, systemic vascular resistance, pulmonary capillary wedge pressure and mean arterial pressure, respectively. Our data implicates a role for myoglobin deficiency in the pathogenesis of congestive heart failure and in the predisposition of doberman pinschers to dilated cardiomyopathy.
J Mol Cell Cardiol 1992 Jul
PMID:Myocardial myoglobin deficiency in various animal models of congestive heart failure. 140 11

In order to assess the development of tolerance we analyzed in a placebo-controlled study the effect of monotherapy with isosorbide-5-mononitrate (IS-5-MN) 60 mg in a controlled release formulation (Durules) once-a-day. The IS-5-MN was evaluated after the first dose and after once-a-day therapy for three days in 11 ambulatory patients (10 males, 1 female, aged 54 +/- 9 years) with stable exercise-induced silent myocardial ischaemia and significant coronary stenoses. The drug was given at 8 o'clock in the morning, and a bicycle ergometer exercise test was performed after 4 hours. The ST segment depression was evaluated by a computer-assisted system. Standing blood pressure decreased during all three periods of active treatment with IS-5-MN, (in comparison with placebo p < 0.001 and p < 0.01, p < 0.01 respectively). Heart rate did not change significantly. Compared with placebo baseline values, ischaemic threshold increased during the first day of treatment (188 sec, p < 0.0001 at 4 hours), and to a lesser extent both in second (103 sec, p < 0.003) and third day (116 sec, p < 0.003). The total exercise time increased during all three days of active therapy but significantly so only during the first day. The exercise stress test performed in the 5th day during placebo demonstrated a high reproducibility of ischaemic-threshold (235 vs 241 sec, p: ns), implying that the improvement during the active treatment with IS-5-MN was not due to a "training effect". Headache in 2 patients was the only significant side-effect.(ABSTRACT TRUNCATED AT 250 WORDS)
G Ital Cardiol 1992 May
PMID:[Lack of tolerance after administration of delayed-action isosorbide-5-mononitrate for 3 days in patients with exercise-induced silent ischemia: control with placebo]. 142 92

We studied 12 patients with stable effort angina in a randomized, double-blind, cross-over and placebo-controlled trial to compare the different antianginal efficacy of "acute" and "chronic" (after reaching a steady-state level) gallopamil therapy. Efficacy was assessed using treadmill exercise testing (Bruce protocol) after a 50 mg single-dose and at the end of a nine-dose course of 50 mg of gallopamil (given three times a day). Three daily exercise tests were performed the first, second, fifth and eighth day of the study protocol at 8, 12 and 16 h. Four hours after a single-dose of gallopamil 50 mg both angina-free exercise time and time to 1 mm ST segment depression increased by a mean value of 78 s (p < 0.003) and 53 s (p < 0.03), respectively, with respect to placebo values. Under steady-state conditions exercise time and time to 1 mm ST segment depression increased by a mean value of 59 s (p < 0.009) and 46 s (p < 0.015), respectively, 4 h after the last dose. The duration of the anti-ischemic effects was no longer present after 8 h for both treatment schedules. Furthermore no significant differences were observed on parameters of ischemia after a single dose as compared to "chronic" therapy. The results of this study reveal that, in accordance with the pharmacodynamic properties of the drug, the anti-ischemic efficacy of 50 mg of gallopamil remains for approximately 4 h. Reaching a steady-state condition does not imply a prolongation of the anti-ischemic effect.
Int J Cardiol 1992 Oct
PMID:Comparison of acute and steady-state conditions of gallopamil therapy in stable angina pectoris. 142 94

Nitrate monotherapy was assessed by treadmill exercise stress testing in 18 patients with significant but relatively asymptomatic myocardial ischemia who were receiving no other antianginal therapy. In addition, prolonged ambulatory electrocardiographic monitoring was performed in 7 patients with demonstrable ischemia during baseline monitoring. After baseline assessment, 5 treatment periods were used in a random order (each of 1 week duration), incorporating 2 dose levels of transdermal nitrate (10 and 20 mg/24 hours) and isosorbide dinitrate (ISDN) (30 and 60 mg/day in divided doses) with a 10-hour nitrate-free interval every 24 hours, as well as a placebo period using a double-blind technique. All treatment periods (including placebo) showed a significant (p < 0.01) 45 to 69% prolongation in the time to 1 mm ST depression during exercise. Paired baseline times of 231 +/- 28 and 233 +/- 30 seconds increased to 367 +/- 37 seconds with 30 mg/day of ISDN, 393 +/- 37 seconds with 60 mg/day of ISDN, 381 +/- 31 seconds with 10 mg/day of transdermal nitrate, and 372 +/- 33 seconds with 20 mg/day of transdermal nitrate. The value for placebo was 342 +/- 29 seconds, which was not significantly different from active treatment (p > 0.1). Some patients appeared to individually respond to > or = 1 nitrate preparation significantly more than to placebo, but this appeared to be unpredictable and largely independent of dosage level and route of administration. There was a qualitatively similar but statistically insignificant reduction in total ischemic time during ambulatory monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1992 Nov 15
PMID:Placebo effect of nitrate monotherapy for myocardial ischemia. 144 72

The role of myocardial oxygen demand in the pathogenesis of silent ambulatory myocardial ischemia was evaluated by reviewing and assessing the methods and results of recent studies. The performance of simultaneous ambulatory electrocardiographic and blood pressure monitoring in 25 men with proven coronary artery disease (CAD) revealed significant increases in heart rate and blood pressure (p < 0.001) preceding most silent ischemic events. By plotting the mean heart rate obtained at 5-minute intervals during the 30 minutes before an ischemic event, the ischemic heart rate was shown to be significantly higher (95 +/- 15 vs 74 +/- 11 beats per minute [bpm]; p < 0.01) than the nonischemic heart rate. The evaluation of heart rate changes during ambulatory ischemia (in patients with CAD and ischemia induced by an exercise test using gradual work load increments) showed a significant heart rate increase (> 10 bpm) at 1-5 minutes preceding the onset of ST-segment depression. Heart rate increases during exercise testing according to the gradual work load increments of the National Institutes of Health protocol were compared with the heart rate preceding ischemic events during daily life monitored by ambulatory electrocardiography and were found to be closely related. In contrast, heart rate increases that occurred during exercise testing using the standard Bruce protocol were higher and correlated less with those preceding ischemia in daily life. Heart rate and blood pressure increased significantly in most silent ischemic episodes, indicating that increased myocardial oxygen demand plays a significant role in the pathogenesis of myocardial ischemia during daily life.
Am J Cardiol 1992 Nov 16
PMID:Role of myocardial oxygen demand in the pathogenesis of silent ischemia during daily life. 144 97

The prevalence and prognostic significance of transient myocardial ischemia after coronary artery bypass grafting (CABG) were evaluated. In 3 studies, ischemia was found in an average of 24% of patients by ambulatory electrocardiographic monitoring at 3-12 months after CABG. An average of 36% of patients in 3 other studies experienced ischemic ST-segment depression during exercise testing at 4-50 months after CABG. Of the ischemic episodes, 77% were silent during exercise testing. In the Coronary Artery Surgery Study (CASS) randomized patient subsets, survival at 12 years was significantly lower for patients who had either silent or symptomatic ischemia during exercise testing at 6 months after CABG compared with those who had no ischemia.
Am J Cardiol 1992 Nov 16
PMID:Significance of silent myocardial ischemia after coronary artery bypass surgery. 144

Episodes of ST depression are closely related to transient decreases in regional myocardial perfusion during physical or mental stress. At the onset of these events, there is transient constriction of atherosclerotic stenoses, with an increase in myocardial demand as reflected by increases in heart rate and blood pressure. Recent research has shown that normal epicardial coronary arteries respond to these provocations and to increasing blood flow with progressive vasodilation. In contrast, atherosclerotic vessels lose this ability to dilate and may show paradoxical constriction. This abnormal constriction parallels the response of the arteries to acetylcholine, which can be used to assess the ability of the coronary endothelium to regulate vasodilation. The loss of endothelium-dependent vasodilation appears to be an important functional manifestation of coronary atherosclerosis and a potential triggering mechanism for transient ischemia. Dysfunctional endothelium may also result in a procoagulant surface, with cell adherence and local thrombus formation. Restoration of normal endothelial function is likely to emerge as an important therapeutic objective in the management of myocardial ischemia and coronary atherosclerosis.
Am J Cardiol 1992 Nov 27
PMID:New insights into the management of myocardial ischemia. 144 5

Serial electrocardiograms as well as echocardiographic studies of 51 pilgrims suffering from acute heat stroke (mean rectal temperature 41.6 degrees C) were performed. All patients were examined immediately after cooling and 24 h later whenever possible. Regional wall motion abnormalities were detected in 9 cases (17.6%) while pericardial effusion was observed in 13 cases (25%) and asymmetrical septal hypertrophy was detected in 8 cases (15.6%). Other cardiac abnormalities included right ventricular dilatation and increased in left ventricular internal dimensions in 4 cases (7.8%), respectively. Thirteen cases (25.5%) had normal echocardiographic findings. Forty (78%) patients had sinus tachycardia while 8 cases (15.7%) showed atrial fibrillation with uncontrolled ventricular rate, and 3 (5.8%) had sinus bradycardia. Heat stroke electrocardiograms showed tracings demonstrating ST segment depression, compatible with ischaemia in 9 cases, while in 6 cases there were nonspecific T wave changes, whereas in another 4 cases the tracings demonstrated different conduction abnormalities. The collected data were analysed and compared to those of 43 control patients. The adverse effects of heat stroke on the heart are multifactorial requiring the utmost attention and understanding, as they reflect the patient's cardiovascular status.
Int J Cardiol 1992 Nov
PMID:Non-invasive evaluation of cardiac abnormalities in heat stroke pilgrims. 145 70

The aim of this study was to analyze the relationship between heart rate and QT interval (HR-QT) during exercise in control subjects (Group A) and in patients with coronary artery disease (CAD) with effort angina and without previous myocardial infarction (MI) (Group B). The diagnosis of CAD was confirmed by coronarographic examination. The correlation HR-QT was significant (p < 0.001) in both groups on effort and at recovery. The analysis of the regression HR-QT was carried out separately, both on effort in upright position and at rest in supine position, to avoid the influence of posture on QT length. During effort, the regression line showed lower slope and intercept values in Group B (p < 0.001) than those for Group A. A similar behavior was also observed at rest. Thus, at the highest heart rate, where ECG signs of ischemia (ST depression > 1 mm) frequently occurred, a longer QT interval was present in Group B. Moreover, in Group B, the QT interval in the presence of ECG signs of ischemia was significantly longer (p < 0.01) than in Group A at comparable heart rates both on effort and at rest, thereby confirming the result obtained by comparing both regression lines. The same effort protocol was repeated in Group B patients after acute administration of atenolol 100 mg per os. After atenolol administration, the analysis of the regression HR-QT in Group B clearly showed a shorter QT interval than that obtained in washout period during the baseline test at the highest heart rates where the ECG frequently showed signs of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Clin Cardiol 1992 Dec
PMID:Influence of atenolol on the relationship between heart rate and QT interval in patients with exercise-induced myocardial ischemia. 147 7


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