Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Maximal changes in haemodynamics and segmental wall motion were seen 2 min after coronary occlusion and were examined in relation to the loading conditions of the left ventricle before occlusion in 20 open chest dogs. There was a significant inverse relationship between the preligation mean aortic pressure and the percentage decrease in stroke volume following ligation. This relationship was observed whether afterload was distributed randomly (mean aortic pressure ranging from 9.7 to 17.6 kPa [73 to 132 mmHg]) between all dogs (r = 0.65; P less than 0.001) or altered by methoxamine (+4 kPa [+30 mmHg]) and nitroprusside (-3.2 kPa [-24 mmHg]) within the same dog (r = 0.82; P less than 0.001; n = 8). Although occlusion of the anterior descending artery caused a small (+5.5%) but significant increase in end-diastolic length of the non-ischaemic epicardial segment, the capacity for compensatory ventricular dilatation was not dependent on preligation afterload. However, the capacity of the ischaemic segment to undergo systolic expansion was significantly greater (+30.2% of end-systolic segment length) in those dogs with the lowest preligation MAP (8 to 12 kPa [60 to 90 mmHg]) compared with systolic lengthening of only 15.8% in the high afterload group (15 to 18 kPa [112 to 135 mmHg]). These data indicate that the loading conditions of the left ventricle predetermine the extent of global and segmental left ventricular dysfunction during the early phase of acute ischaemic injury.
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PMID:Afterload as a predeterminant of haemodynamics and segmental wall motion following coronary artery occlusion. 47 39

Infarct expansion remains an important sequela of myocardial infarction. Both angiotensin converting enzyme inhibitors and intravenous nitrates reduce early infarct expansion in humans. This is believed to be caused by the reduction in left ventricular systolic wall stress that results from the arteriolar vasodilatation they produce. Patients are frequently already receiving calcium channel blockers at the time of infarction or these drugs are sometimes administered in the perimyocardial infarction period. The calcium blockers of the dihydropyridine class might be expected to modify infarct expansion. However, their effect on this process has not been studied. We therefore evaluated the effect of early treatment with the calcium blocker amlodipine, a potent arteriolar vasodilator with minimal negative inotropic properties, on chronic myocardial infarction in the rat. Permanent left coronary occlusion was created after pretreatment with amlodipine, 0.25 mg/kg (low dose) or 1.0 mg/kg (high dose), or placebo, intravenously twice a day, and continued for 7 days after infarction. Hearts (n = 50) were perfusion fixed 21 days after infarction and analyzed for infarct extent, scar thickness, left ventricular shape and size, and expansion index. Both doses decreased mean blood pressure (119 +/- 3 to 99 +/- 5 mm Hg low dose, p = 0.004; 110 +/- 5 to 84 +/- 4 mm Hg high dose, p = 0.0003), with reflex tachycardia only after the high dose (heart rate 395 +/- 9 to 434 +/- 11, p = 0.001). Infarct extent was equal in the three groups (39 +/- 2%, 41 +/- 2%, and 41 +/- 3% of left ventricular circumference for control, low, and high doses, respectively). The three groups did not differ significantly with regard to left ventricular cavity cross-sectional area (80 +/- 4, 77 +/- 3, and 87 +/- 3 mm2, control, low, and high doses, respectively; p = 0.07 high dose vs control), mean scar thickness (0.74 +/- 0.06, 0.73 +/- 0.05, and 0.65 +/- 0.06 mm, control, low, and high doses, respectively; p = NS), and expansion index (1.52 +/- 0.10, 1.58 +/- 0.12, and 1.95 +/- 0.19, control, low, and high doses, respectively; p = 0.08 high dose vs control). In the subgroup with larger infarcts (infarct extent greater than 0.39 of left ventricle), the expansion index was higher in the high-dose group (2.37 +/- 0.23 vs 1.64 +/- 0.17 control; p = 0.04). In this model, treatment with amlodipine does not limit infarct extent or reduce early infarct expansion and left ventricular dilatation, even when initiated before infarction.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of amlodipine on myocardial infarction, infarct expansion, and ventricular geometry in the rat. 138 6

In the first few hours after the onset of coronary occlusion the infarct zone stretches due to myocyte slippage. Subsequently the noninfarct zone develops volume overload hypertrophy with series addition of new sarcomeres and fibre elongation. Dilatation is detrimental as it increases ventricular wall stress and oxygen demand, and re-entry of electrical impulses may be influenced by stretching of the ischaemic scar resulting in ventricular fibrillation. Left ventricular remodelling and dilatation is a progressive process which begins early and continues in the months after infarction. The major determinants of the extent of remodelling are infarct size and patency of the infarct-related artery. Late reperfusion may reverse initial infarct dilatation and decrease left ventricular volumes by inducing calcium-activated contracture of the actomyosin complex. Expansion may also be inhibited by acceleration of healing, splinting of the infarct zone by salvage of subepicardial cells, and blood in the coronary arteries and veins supporting the infarct zone. End-systolic volume is the strongest predictor of long-term prognosis after infarction. A number of therapies including thrombolysis, angiotensin-converting enzyme (ACE) inhibition and nitrates have been shown to decrease left ventricular dilatation. The optimal time for commencement, dose, duration and the effects of combinations of therapy are yet to be determined.
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PMID:Remodelling of the heart after myocardial infarction. 144 47

Cardiac function in myocardial infarction (MI) depends on the extent of damage in ischemic myocardium and the compensatory response of residual myocardium. Because thrombolytic therapy is performed in many patients, reperfusion of ischemic myocardium may take place at various stages of progression of the ischemic insult. If perfusion is reestablished before necrosis occurs, myocardium may recover immediately or after hours to weeks ("stunned myocardium"). If coronary occlusion persists, necrosis develops in the subendocardium, propagates transmurally and forms a scar after the healing phase. Residual myocardium responds to loss of contractile tissue and material properties of the ischemic zone by hypertrophy and dilatation. This study shows that left ventricular dilatation is accompanied by an increase in stroke volume from 4 days to 4 weeks; however, left ventricular dilatation progresses while stroke volume remains constant from 4 weeks to 6 months, suggestive of noncompensatory left ventricular dilatation. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce lactate production after 60 seconds, and infarct size after 6 hours of coronary occlusion in dogs. Stunned myocardium recovers faster in animal experiments and pacing-induced myocardial ischemia may be prevented by ACE inhibitors. Left ventricular dilatation and mortality is reduced by ACE inhibitors in rats after MI. Several potential mechanisms are discussed to establish a favorable action of ACE inhibitors at various stages of MI. Clinical evidence is still pending; however, large studies are ongoing to clarify potential indications of ACE inhibitors in ischemic heart disease in humans.
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PMID:Influence of angiotensin-converting enzyme inhibition on cardiac function in myocardial infarction. 218 51

In order to study myocardial and clinical events during transient coronary occlusion in humans, two-dimensional echocardiography was continuously performed in 15 patients undergoing 49 balloon inflations during percutaneous transluminal coronary angioplasty (PTCA). Transient segmental asynergy developed in all patients 8 +/- 3 seconds after balloon inflation and returned to baseline 19 +/- 8 seconds after balloon deflation. Segmental dyskinesis was seen in only 8 of 11 patients undergoing PTCA of the left anterior descending artery (LAD). A wall motion score, based on degree of asynergy of 13 segments of the left ventricle, was significantly higher during LAD than during right coronary artery inflation (7.9 +/- 1.3 vs 4.0 +/- 1.4, p less than 0.01). Left ventricular size index increased significantly during balloon inflation, from 179 +/- 9 to 196 +/- 10 mm (p less than 0.01). Four patients developed transient ST segment changes in the extremity leads of the ECG and five patients had angina pectoris. The very first sign of ischemia in three patients, who developed all of these symptoms together, was consistently asynergy, followed by ECG changes, and last, angina pectoris. Thus during PTCA, transient asynergy and left ventricular dilatation develop, which are often clinically silent.
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PMID:Two-dimensional echocardiography during percutaneous transluminal coronary angioplasty. 294 Aug 52

Myocardial infarction following coronary occlusion limits the effectiveness of emergency coronary artery bypass operations. We designed and evaluated a transvenously introduced balloon-tipped catheter and an electrocardiogram-activated pumping system for perfusing ischemic myocardium by retrograde pulsation of oxygenated blood into the coronary veins during diastole. Balloon deflation during systole allowed for normal venous drainage. Four groups of dogs (n = 26) were instrumented with sonomicrometry crystals and catheters to measure regional and global left ventricular function. Two groups of dogs had chronic left ventricular (LVH) produced by prior aortic banding (left ventricular mass 174 gm versus 115 gm for control dogs of equal body weight, p less than or equal to 0.05). The left anterior descending coronary artery (LAD) was occluded for 40 minutes; after 10 minutes left ventricular function was severely depressed in all groups (less than or equal to 0.05 compared to baseline). Groups 1 (normal left ventricle, n = 8) and 2 (LVH, n = 5) had no further therapy for the following 30 minutes. Groups 3 (normal left ventricle, n = 8) and 4 (LVH, n = 5) received 30 minutes of coronary vein retroperfusion (CVRP) 10 minutes following the LAD occlusion. CVRP restored 37% of systolic shortening, whereas there was no restoration of systolic shortening in control dogs (p less than or equal to 0.001). All other physiological and hemodynamic parameters including heart rate, cardiac output, aortic pressure, dP/dt, and left ventricular dilatation were normalized during CVRP while remaining severely depressed in control dogs (p less than or equal to 0.05). Following restoration of arterial flow at 40 minutes, 10 of 13 CVRP-treated dogs recovered normal left ventricular function while only two of 13 untreated dogs survived. CVRP offers a transvenous approach for modifying myocardial ischemia prior to emergency coronary artery bypass grafting.
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PMID:Modification of myocardial ischemia in normal and hypertrophied hearts utilizing diastolic retroperfusion of the coronary veins. 621 Aug 8

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

Because the small leucine-rich proteoglycan decorin has been implicated in regulation of collagen fibrillogenesis leading to proper extracellular matrix assembly, we hypothesized it could play a key role in cardiac fibrosis following myocardial infarction. In this study we ligated the left anterior descending coronary artery in wildtype and decorin-null mice to produce large infarcts in the anterior wall of the left ventricle. At early stages post-coronary occlusion the myocardial infarction size did not appreciably differ between the two genotypes. However, we found a wider distribution of collagen fibril sizes with less organization and loose packing in mature scar from decorin-null mice. Thus, we tested the hypothesis that these abnormal collagen fibrils would adversely affect post-infarction mechanics and ventricular remodeling. Indeed, scar size, right ventricular remote hypertrophy, and left ventricular dilatation were greater in decorin-null animals compared with wildtype littermates 14 days after acute myocardial infarction. Echocardiography revealed depressed left ventricular systolic function between 4 and 8 weeks post-ischemia in the decorin-null animals. These changes indicate that decorin is required for the proper fibrotic evolution of myocardial infarctions, and that its absence leads to abnormal scar tissue formation. This might contribute to aneurysmal ventricular dilatation, remote hypertrophy, and depressed ventricular function.
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PMID:A role for decorin in the remodeling of myocardial infarction. 1594 32

Two features of off-pump coronary artery bypass (OPCAB) can lead to hemodynamic instability: transient occlusion of coronary arteries during distal anastomosis construction and displacement of the heart to provide access to distal coronary arteries. The position of the heart during OPCAB trans-esophageal echocardiography (TEE) can often provide an indication as to how much compression of the right or left ventricle has occurred. If either chamber is not filling, repositioning of the heart will be necessary. Close observation of the heart with TEE during periods of coronary occlusion may facilitate detection of worsening cardiac function as evidenced by weakening contraction, ventricular dilatation, or increasing mitral or tricuspid regurgitation. Haemodynamic changes are more pronounced with displacement of the heart to access posterior coronary arteries than anterior vessels. Cardiac manipulations during off-pump coronary artery bypass grafting (OPCABG) can lead to haemodynamic instability. This, along with distal anastomosis causing transient occlusion of coronary arteries, may cause transient hypotension with increased filling pressures. TEE is more helpful in this scenario. In these patients, TEE helps differentiate between cardiac dysfunction and secondary to myocardial ischemia in which regional wall motion abnormalities will be present from a much more common scenario where the increase in filling pressure is secondary to extra cardiac compression and provides the ability to detect mitral regurgitation (MR) with a color-flow Doppler, as well as assess right heart function.
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PMID:Trans-esophageal echocardiography in off-pump coronary artery bypass grafting. 1960 50

Myocardial infarction remains a major health-related problem with significant acute and long-term consequences. Acute coronary occlusion results in marked electrophysiologic alterations that can induce ventricular tachyarrhythmias such as ventricular tachycardia or ventricular fibrillation, often heralding sudden cardiac death. During the infarct-healing stage, hemodynamic and structural changes can lead to left ventricular dilatation and dysfunction, whereas the accompanying fibrosis forms the substrate for re-entrant circuits that can sustain ventricular tachyarrhythmias. A substantial proportion of such patients present clinically with overt heart failure, a common disease-entity associated with high morbidity and mortality. Several lines of evidence point toward a key role of the growth hormone/insulin-like growth factor-1 axis in the pathophysiology of post-infarction structural and electrophysiologic remodeling. Based on this rationale, experimental studies in animal models have demonstrated attenuated dilatation and improved systolic function after growth hormone administration. In addition to ameliorating wall-stress and preserving the peri-infarct myocardium, antiarrhythmic actions were also evident after such treatment, but the precise underlying mechanisms remain poorly understood. The present article summarizes the acute and chronic actions of systemic and local growth hormone administration in the post-infarction setting, placing emphasis on the electrophysiologic effects. Experimental and clinical data are reviewed, and hypotheses on potential mechanisms of action are discussed. Such information may prove useful in formulating new research questions and designing new studies that are expected to increase the translational value of growth hormone therapy after acute myocardial infarction.
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PMID:Electrophysiologic Effects of Growth Hormone Post-Myocardial Infarction. 3201 45


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