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)

Changes of ischemic myocardium following coronary occlusion, including active and passive functions, and adaptive changes of non-ischemic surviving myocardium have been summarized under the term "left ventricular remodeling" post myocardial infarction. An increase in left ventricular volume may be a consequence, and associated with an adverse prognosis. Although left ventricular dilatation may increase stroke volume and, thus, be compensatory at first, in about one-fifth of patients it ultimately results in progressive dysfunction and heart failure. Major determinants of this process are time, infarct size, infarct location, global left ventricular function assessed 4 days after infarction by radionuclide ejection fraction and right heart catheter (stroke volume), and morphology of the infarct-associated coronary artery. The surviving myocardium hypertrophies and may also dilate structurally. Depression of left ventricular ejection fraction chronically after the infarct is due to deterioration of wall motion of chamber segments initially classified normal by radionuclide analysis. Biochemical changes may also occur, including reduction of phosphocreatine, prolongation of time to peak Cai2+, and changes in myosin isoforms. Systemic or local humoral factors may be involved in these changes, however, clear evidence is still lacking. Perfusion of surviving myocardium may be altered under various conditions due to morphologic and functional changes of coronary vasculature. Successful prevention of heart failure and death by angiotensin converting enzyme inhibitors in asymptomatic patients with left ventricular dysfunction post-myocardial infarction has supported the pathophysiologic concepts of remodeling.
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PMID:Ventricular remodeling after myocardial infarction. Experimental and clinical studies. 835 28

1. The effect of R75231, an inhibitor of purine nucleoside transport, were examined on ischaemic arrhythmias in anaesthetized pigs. 2. In closed chest pigs (n = 4), R75231 exerted a moderate dose-dependent decrease in mean arterial blood pressure (from 97 +/- 4 mmHg to 95 +/- 4, 90 +/- 1 and 83 +/- 2 mmHg at 25, 50 and 100 micrograms kg-1 respectively) and produced a dose-related shift to the left of the blood pressure dose-response curve to intravenous bolus doses of adenosine. The degree of inhibition of adenosine uptake by R75231, assessed ex vivo in erythrocyte suspensions, was 43 +/- 5%, 64 +/- 13 and 114 +/- 15% at doses of 25, 50 and 100 micrograms kg-1 respectively. 3. In open chest pigs, intravenous injection of R75231 (50 micrograms kg-1; n = 6 and 100 micrograms kg-1; n = 10) induced a dose-related decrease in both systolic and diastolic arterial blood pressure which was more marked than in closed-chest pigs (mean pressure 86 +/- 4 to 70 +/- 2 mmHg and 88 +/- 6 to 60 +/- 6 mmHg with 50 and 100 micrograms kg-1 respectively), without affecting heart rate or myocardial contractility. Coronary artery occlusion in these pigs caused a secondary decrease in blood pressure. This was not observed in controls (n = 10). The lower dose of R75231 did not exert any antifibrillatory effects, whereas the higher dose significantly reduced the incidence of ventricular fibrillation, from 80% in control pigs to 30%. Neither dose modified the incidence of ventricular tachycardia (33% and 40% with 50 and 100 microg kg-1 respectively, compared to 30% in controls) or had any effect on the total number of ventricular ectopic beats (85 +/- 47 and 130 +/- 31 vs 110 +/- 19 in controls). R75231, at a dose of 100 microg kg-1, also attenuated the ischaemia-induced shortening of QRS-interval, but neither dose modified the ST-segment depression seen following occlusion.4. These results show that the nucleoside transport inhibitor, R75231, exerts an antifibrillatory effect ina model of severe myocardial ischaemia in a dose which completely inhibits adenosine uptake ex vivo.However, while this agent has minimal haemodynamic effects in closed chest animals, the reduction in blood pressure induced by R75231 in open-chest pigs cannot be excluded as a possible contributory mechanism of the antiarrhythmic effects of this drug.
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PMID:The antiarrhythmic effects of the nucleoside transporter inhibitor, R75231, in anaesthetized pigs. 835 59

The mechanism and significance of precordial ST depression during inferior wall acute myocardial infarction (AMI) is debated. This study assessed the location and extent of arterial perfusion distribution responsible for this electrocardiographic finding. Intracoronary thallium-201 was injected in 11 patients with 1-vessel right coronary disease to delineate perfusion distribution that was quantitated by a new angiographic distribution score. The angiographic score correlated with posterior (r = 0.84), posterolateral (r = 0.88) and total (r = 0.73) extent of intracoronary thallium distribution. The angiographic distribution score was related to electrocardiographic changes in 16 patients showing an inferior ST-segment elevation during angioplasty (7 with and 9 without precordial ST depression), of which 6 received intracoronary thallium injection. None had thallium distribution in the anterior or septal segment, but there was a trend toward a greater angiographic distribution score and posterior segment thallium score in patients with precordial ST depression. In another 77 patients with inferior wall AMI due to right coronary occlusion (24 with concomitant left anterior descending narrowing), precordial ST depression was present in 16 with and 31 without left anterior descending narrowing (p = NS). The angiographic distribution score was higher in those with than without precordial ST depression (0.59 +/- 0.10 vs 0.44 +/- 0.11, p < 0.001) in both patients with and without left anterior descending disease. The magnitude of both inferior ST elevation and precordial ST depression correlated with the angiographic distribution score, but only precordial ST depression was independently related in multivariate analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism and significance of precordial ST-segment depression during inferior wall acute myocardial infarction associated with severe narrowing of the dominant right coronary artery. 847 63

Differentiation between left circumflex occlusion and right coronary occlusion in inferior acute myocardial infarction is a common clinical problem. This study investigated new electrocardiographic markers for differentiation, including T wave inversion, and individual inferior and precordial lead ST level, versus the traditional criterion of lateral ST elevation. In 95 angiographically characterised patients, ST elevation in lateral chest lead V5 or V6 had a sensitivity of 56% and specificity of 92% to predict left circumflex related acute myocardial infarction while the absence of lateral T inversion in I and AVL was even more sensitive (89%) though less specific (74%). A criterion of ST depression in V1 > 0.1 mV has a sensitivity of 61% and specificity of 84% whereas a criterion of ST level in III minus II < or = 0.1 mV has a sensitivity of 94% and specificity of 37% in predicting left circumflex related acute myocardial infarction. These criteria were then tested in another 49 patients subsequently recruited with inferior acute myocardial infarction. Useful parameters that discriminated left circumflex related acute myocardial infarction from right coronary related acute myocardial infarction include lateral ST elevation (38% vs. 7%, P < 0.05), absence of lateral T inversion (50% vs. 15%, P < 0.05), and ST depression in V1 of more than 0.1 mV (50% vs. 7%, P < 0.05). The present study revealed new electrocardiographic clues to suggest a left circumflex related inferior acute myocardial infarction other than lateral ST elevation. However, it should be noted that no single electrocardiographic variable or their combinations could identify the infarct-related artery with complete certainty.
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PMID:Electrocardiographic identification of the infarct-related artery in acute inferior myocardial infarction. 879 79

Repeated short episodes of coronary occlusion in experimental animals, and in humans during balloon angioplasty, cause myocardial preconditioning. This study examines whether myocardial ischemia induced by repeated exercise testing can reduce the extent of ischemia induced by subsequent exercise tests. Twenty-six patients with positive stress tests underwent 3 treadmill exercise tests at 30-minute intervals. Two additional tests were performed on each of the previous 2 days in order to eliminate and/or reduce the training effect. All 3 exercise tests were of similar work load. In spite of that, total ischemic time was markedly shortened from 633 to 399 seconds (p <0.0001) as well as the recovery time from 259 to 126 seconds (p <0.0001) between the first and the second tests. There was no further improvement on the third test. Time to 1-mm ST depression was prolonged from 487 to 593 seconds (p = 0.004) and double product at 1-mm ST depression was increased in the second test from 20,322 to 22,325 mm Hg/second (p = 0.008), implying a higher ischemic threshold. An improvement of > or = 10% in < or = 1 ischemic parameter was observed in 25 of the 26 patients and in > or = 2 of the ischemic parameters in 76% of the patients. Improvement in ischemic parameters develops during repeated exercise induced ischemia in most patients. We suggest that this phenomenon, which was previously known as "warm up," is the clinical counterpart of myocardial preconditioning which develops not only during ischemia caused by reduction in coronary flow, but also during demand-induced ischemia.
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PMID:Improvement in ischemic parameters during repeated exercise testing: a possible model for myocardial preconditioning. 891 68

In order to examine the status of G-proteins in congestive heart failure due to myocardial infarction, the left coronary artery in rats was ligated and animals assessed after 4, 8 and 16 weeks. Sham-operated control and experimental animals were used for the preparation of membranes from the viable (uninfarcted) left and right ventricles. Adenylyl cyclase activities in the presence of pertussis toxin and cholera toxin were increased and decreased in left ventricles from all groups, respectively. On the other hand, adenylyl cyclase activities in 8 and 16-week experimental right ventricles were unaltered in the presence of pertussis toxin and increased in the presence of cholera toxin. Depression of adenylyl cyclase activities in left ventricles from all groups as well as in the right ventricle at 4 weeks were not evident when enzyme activity was determined in the pertussis toxin-treated membranes in the absence or presence of Gpp(NH)p. Cholera toxin-catalyzed ADP ribosylation was decreased in left ventricles from all infarcted groups and increased in the right ventricles at 8 and 16 weeks whereas the pertussis toxin-catalyzed ADP ribosylation was increased in all experimental tissues except in the right ventricles at 8 and 16 weeks. G(s alpha)-protein content was decreased in the left ventricle at 16 weeks and increased in the right ventricles at 8 and 16 weeks of myocardial infarction. On the other hand, G(i alpha)-protein content was increased in left ventricles from all infarcted groups and the 4-week right ventricle but was unaltered in 8 and 16-week right ventricles. An increase in mRNA abundance for G(i alpha)-protein was seen in both left and right ventricles following myocardial infarction. A significant increase in mRNA level for G(s alpha)-protein was observed in all left ventricles and 8-week right ventricle following the coronary occlusion. These results suggest that changes in Gs- and Gi-proteins in the failing heart due to myocardial infarction are chamber-specific and are dependent upon the stage of congestive heart failure.
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PMID:Differential alterations in left and right ventricular G-proteins in congestive heart failure due to myocardial infarction. 992 53

ATP-sensitive potassium (K(ATP)) channels are activated during myocardial ischemia. The ensuing potassium efflux leads to a shortening of the action potential duration and depolarization of the membrane by accumulation of extracellular potassium favoring the development of reentrant arrhythmias, including ventricular fibrillation. The sulfonylthiourea HMR 1883 was designed as a cardioselective blocker of myocardial K(ATP) channels for the prevention of arrhythmic sudden death in patients with ischemic heart disease. We investigated the effect of HMR 1883 on sudden cardiac arrhythmic death and electrocardiography (ECG) changes induced by 20 min of left anterior descending coronary artery occlusion in pentobarbital-anesthetized pigs. HMR 1883 (3 mg/kg i.v.) protected pigs from arrhythmic death (91% survival rate versus 33% in control animals; n = 12; p<.05). Ischemic areas were of a similar size. The compound had no effect on hemodynamics and ECG, including Q-T interval, under baseline conditions and no effect on hemodynamics during occlusion. In control animals, left anterior descending coronary artery occlusion lead to a prompt and significant depression of the S-T segment (-0.35 mV) and a prolongation of the Q-J time (+46 ms), the former reflecting heterogeneity in the plateau phase of the action potentials and the latter reflecting irregular impulse propagation and delayed ventricular activation. Both ischemic ECG changes were significantly attenuated by HMR 1883 (S-T segment, -0.14 mV; Q-J time, +15 ms), indicating the importance of K(ATP) channels in the genesis of these changes. In conclusion, the K(ATP) channel blocker HMR 1883, which had no effect on hemodynamics and ECG under baseline conditions, reduced the extent of ischemic ECG changes and sudden death due to ventricular fibrillation during coronary occlusion.
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PMID:ATP-sensitive potassium channel blocker HMR 1883 reduces mortality and ischemia-associated electrocardiographic changes in pigs with coronary occlusion. 1052 61

Kornreich identified 6 body surface potential mapping (BSPM) leads outside the standard 12-lead electrocardiographic (ECG) sites for optimal recognition of ST segment elevation (+) and depression (-) during acute ischemia in anterior, inferior, and posterior myocardial zones (A+, A-, I+, I-, P+, P-). No comparison has been made between the 6 selected BSPM leads and 18-lead ECG (12 + V3-5R + V7-9) in detecting acute myocardial ischemia during coronary occlusion. Continuous 18-lead ECG and 6 selected BSPM leads were recorded in 68 patients (77 vessels) undergoing coronary angioplasty during balloon occlusion. Ischemia was defined as ST segment deviation (deltaST) > or = 100 microV > or = 1 lead from the preinflation baseline. The 18-lead ECG was a more frequent source of the maximal deltaST lead during left anterior descending artery, right coronary artery, and left circumflex artery occlusion (71 [92%]) than the 6 selected BSPM leads (5 [7%]). The 18-lead ECG was more efficacious than the 6 selected BSPM leads for detecting acute myocardial ischemia in the group as whole. The 18-lead ECG was also more efficacious for detecting right ventricular ischemia associated with proximal right coronary artery occlusion and for detecting ST segment elevation during left circumflex artery occlusion. Our findings indicate that the 18-lead ECG is the most frequent source of maximally deviated lead and is more efficacious in detecting myocardial ischemia during balloon occlusion than the 6 selected BSPM leads. The 6 selected BSPM leads do not add information above and beyond the 12- or 18-lead ECG, and thus cannot be recommended as optimal sites for continuous ST segment monitoring of patients with acute coronary syndromes.
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PMID:Comparison of 18-lead ECG and selected body surface potential mapping leads in determining maximally deviated ST lead and efficacy in detecting acute myocardial ischemia during coronary occlusion. 1068

Dobutamine stress echocardiography is widely performed as a useful diagnostic tool in patients with known or suspected coronary artery disease. Dobutamine induced myocardial ischaemia is frequently associated with ST segment depression. ST segment elevation is uncommon and is almost always associated with prior myocardial infarction or transient total coronary occlusion. Dobutamine induced ST segment elevation in absence of significant coronary artery disease is a rare condition and is supposed to be a consequence of severe coronary artery spasm. The case of a 58 year old man with variant angina episodes at rest, during exercise test, and dobutamine stress echocardiography is reported, in whom coronary spasm without significant coronary artery stenoses was documented angiographically.
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PMID:Angiographic documented coronary arterial spasm in absence of critical coronary artery stenoses in a patient with variant angina episodes during exercise and dobutamine stress echocardiography. 1072 56

It is known that T-wave alternans (TWA), which identify patients at risk for arrhythmic events, often occur during acute coronary occlusion in association with ST-segment elevation. To test the hypothesis that TWA is associated with a certain state/severity of myocardial infarction/ischemia, we assessed the association between TWA and ST-segment depression during exercise-induced ambulatory ischemia. Of 351 consecutive patients with coronary artery disease who underwent assessment of microvolt TWA by exercise, 23 patients with effort angina without a history of infarction with ST depression (> or =0.11 mV) during TWA test were selected. These patients were compared with 222 postinfarction patients consisting of 38 patients with, and 184 patients, without the ST depression, and 18 normal individuals. The incidence (9%) of determinate TWA in the patients with angina was significantly (P < .0001) lower than that (52%) in the postinfarction patients. There was no significant difference between the angina patients and the controls (6%). There was also no difference between the patients with (58%) and without the ST depression (51%) in the postinfarction patients. Moreover, no correlation existed between the TWA voltage and the ST-depression magnitude in both angina and postinfarction patients. We concluded that there is no association between TWA and ambulatory ischemia with ST depression.
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PMID:Lack of an association between T-wave alternans and ST-segment depression during exercise-induced ambulatory ischemia. 1095 79


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