Biomedical subjects

B I Jugdutt

Publications and source records attributed to B I Jugdutt.

At least 55 records · Page 3Linked to original sources

PubMed1994

Effect of prolonged nitrate therapy on left ventricular remodeling after canine acute myocardial infarction.

BACKGROUND: Prolonged nitrate therapy during healing between 2 days and 6 weeks after anterior myocardial infarction has the potential for limiting further left ventricular remodeling (or changes in topography) and preserving function. Longterm therapy throughout healing over 6 weeks might be more beneficial than short-term therapy over the first 2 weeks after infarction. METHODS AND RESULTS: The effect of prolonged nitrate therapy between 2 days and 6 weeks during healing after infarction on serial parameters of ventricular remodeling (scar expansion, scar thinning, ventricular dilation, and hypertrophy) and function (asynergy or akinesis plus dyskinesis and ejection fraction) by serial two-dimensional echocardiography, hemodynamics, postmortem topography (computerized planimetry, geometric maps, and radiographs), and collagen content (hydroxyproline) was studied in 64 instrumented dogs randomized 2 days after left anterior descending coronary artery ligation to various nitrate regimens (n = 32) over the first 2 weeks (subgroup 1: 2% transdermal nitroglycerin at 8 AM and 4 PM, n = 6; subgroup 2: 2% transdermal nitroglycerin plus 2.6 mg of sustained-release oral nitroglycerin at 8 AM, 3 PM, and 10 PM, n = 5; subgroup 3: oral isosorbide dinitrate, 30 mg at 8 AM and 4 PM, n = 11) or 6 weeks (subgroup 4: isosorbide dinitrate, n = 10) and in matching controls (n = 32). Nitrate therapy reduced left atrial pressure, mean arterial pressure, and the rate-pressure product compared with controls over the 6 weeks. Postmortem scar mass and hydroxyproline were similar in control and nitrate groups. However, scar stretching and thinning, cavity dilation, noninfarct wall hypertrophy, and apical bulging were less with nitrates, especially in the long-term subgroup 4. In vivo remodeling parameters between 2 days and 6 weeks after ligation showed that, compared with controls, nitrate therapy prevented further stretching of the asynergic segment, decreased the expansion index, decreased further scar thinning, prevented the increase in ventricular volumes, reduced the frequency of ventricular aneurysm, prevented the increase in ventricular mass, reduced the extent of asynergy, and improved ejection fraction. Although the beneficial effect on topography and function was seen in all nitrate subgroups, the overall benefit was greater with long-term therapy over 6 weeks (subgroup 4) than short-term therapy confined to the first 2 weeks (subgroups 1, 2, and 3). CONCLUSIONS: Prolonged nitrate therapy, in various regimens during healing after infarction, effectively reduced left ventricular loading and prevented infarct thinning, further infarct expansion, progressive ventricular dilation, and the increase in mass. These effects were associated with decreased asynergy and improved ejection fraction. The beneficial effects were greater with long-term therapy over 6 weeks than short-term therapy over the first 2 weeks.

Animals↗

PubMed1993

Effects of nitrate therapy on ventricular remodeling and function.

The hypothesis that nitrates might effectively limit left ventricular remodeling and improve function after acute myocardial infarction has been tested in experimental and clinical models, with special attention to the pathophysiologic evolution of remodeling. In 1 clinical study, before the thrombolytic era, the effects of low-dose intravenous nitroglycerin infusion for the first 48 hours during acute myocardial infarction was evaluated in a prospective, randomized, single-blinded, placebo-controlled study of 310 patients (154 nitroglycerin; 156 placebo). Nitroglycerin proved to be safe and produced several benefits compared with placebo: (1) smaller infarct size; (2) less left ventricular dysfunction; (3) less infarct expansion and thinning; (4) better functional status; (5) fewer in-hospital complications such as left ventricular failure, left ventricular thrombus, cardiogenic shock, and infarct extension; and (6) fewer deaths up to 1 year. Two subsequent clinical studies in the thrombolytic era, with low-dose intravenous nitroglycerin infusion during infarction over the first 48 hours followed by buccal nitrate (eccentric dose regimen) or placebo during healing over 6 weeks postinfarction, indicated that prolonged nitrate therapy effectively limited left ventricular remodeling and improved function further compared with placebo.

Heart Ventricles↗

PubMed1993

Intractable ventricular arrhythmias during remodelling and healing after acute myocardial infarction.

A patient with extensive myocardial infarction, evidence of early ventricular remodelling, regional left ventricular (LV) dilation and aneurysm formation developed recurrent ventricular tachyarrhythmias and episodes of sudden death. The patient finally died 24 days post infarction despite effective anti-remodelling therapy and appropriate anti-failure and anti-arrhythmic therapies. Remarkable findings at autopsy included normal LV size and a small LV apical aneurysm despite as much as 52% LV necrosis and further right ventricular necrosis. The case underscores the need for aggressive early infarct-limiting therapy to prevent early remodelling, LV aneurysm and possibly fatal ventricular tachyarrhythmias.

Electrocardiography↗

PubMed1992

Role of nitrates after acute myocardial infarction.

Apart from their ability to relieve myocardial ischemia, nitrates have an important role to play on preservation of left ventricular (LV) geometry and function after acute myocardial infarction (MI). In the first 48 hours after acute MI, intravenous nitroglycerin infusion titrated to a low-dose regimen produces multiple benefits, including smaller infarct size, better regional and global LV function, less remodeling, fewer in-hospital complications, and fewer deaths in-hospital and up to 1 year. This regimen might be an effective adjunct during reperfusion therapy for salvaging ischemic myocardium, LV geometry, and function. Recent studies indicate that prolonged therapy with nitrates during the healing phase after acute MI can effectively further limit progressive LV remodeling (less LV dilation, expansion, thinning, and aneurysm formation) and preserve LV function. Tolerance with chronic therapy is avoided by an eccentric dose regimen to provide a nitrate-free interval.

Drug Administration Schedule↗

PubMed1992

Effect of long-term captopril therapy on left ventricular remodeling and function during healing of canine myocardial infarction.

To determine whether the long-term reduction of preload and afterload by captopril during healing after acute anterior myocardial infarction might attenuate left ventricular remodeling and improve function, 30 chronically instrumented dogs with infarction produced by left anterior descending coronary artery ligation were randomized 2 days later to oral therapy with placebo (n = 15) or captopril, 50 mg twice daily (n = 15), for 6 weeks. Serial hemodynamic as well as topographic and functional variables (two-dimensional echocardiography) were measured over 6 weeks. Scar topography (planimetry), occluded bed size (coronary arteriography) and collagen (hydroxyproline) content were measured at 6 weeks. Between 2 days and 6 weeks, captopril decreased (p less than 0.001) mean arterial pressure and mean left atrial pressure more than did placebo, but it did not influence heart rate. Infarct scar mass, transmurality and collagen content at 6 weeks were similar in the two groups but scars showed less (p less than 0.001) thinning and expansion with captopril than with placebo. Echocardiograms showed similar infarct expansion and thinning in the two groups at 2 days but less aneurysm with captopril at 6 weeks. Between 2 days and 6 weeks, expansion index (infarct-/noninfarct-containing segment length) decreased (p less than 0.001) with captopril but increased (p less than 0.001) with placebo. Also, thinning ratio (infarct/normal wall thickness) decreased (p less than 0.001) with placebo but did not change (p = NS) with captopril. By 6 weeks, left ventricular asynergy and volumes showed a greater decrease (p less than 0.01) and global ejection fraction a greater increase (p less than 0.05) with captopril.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Functional impact of remodeling during healing after non-Q wave versus Q wave anterior myocardial infarction in the dog.

OBJECTIVES: This study was undertaken to compare changes in left ventricular remodeling and function during healing after a first anterior non-Q wave versus a Q wave myocardial infarction in the dog. BACKGROUND: Whether ventricular remodeling is more severe after anterior Q wave than after anterior non-Q wave infarction has not been studied systematically. METHODS: Serial remodeling and functional variables (two-dimensional echocardiography), electrocardiography and hemodynamic data were recorded over 6 weeks in 58 instrumented dogs subjected to left anterior descending coronary artery ligation or ligation plus collateral obliteration. Postmortem topography and transmurality (by planimetry) and infarct collagen (hydroxyproline) were measured at 6 weeks. RESULTS: At 6 weeks, infarct collagen was similarly increased in both groups, but the Q wave group had greater infarct size (7.2% vs. 4.5%, p less than 0.025) and greater transmurality (88% vs. 58%, p less than 0.001), higher left atrial pressures, more infarct expansion (expansion index 2.62 vs. 2.31, p less than 0.001), more thinning (thinning ratio 0.62 vs. 0.72, p less than 0.001), greater cavity dilation (diastolic volume 88 vs. 72 ml, p less than 0.001), more regional bulging in the short-axis view (depth 4.9 vs. 1.9 mm, p less than 0.001), more regional asynergy (18% vs. 7%, p less than 0.001), lower global ejection fraction (40% vs. 48%, p less than 0.001), more endocardial and epicardial bulging in the long-axis view and greater incidence of aneurysm (82% vs. 36%, p less than 0.005), left ventricular thrombus (64% vs. 0%, p less than 0.0005) and ventricular arrhythmias. Echocardiograms obtained during a 6-week period indicated that left ventricular topographic deterioration and dysfunction were present in the earliest postinfarction study at 2 days in both groups but were more frequent in the Q wave group. Regional myocardial blood flow (24 dogs) was lower in the Q wave than in the non-Q wave group. Scanning electron microscopy (10 dogs) revealed preservation of the epicardial collagen matrix in the non-Q wave but not the Q wave group. CONCLUSIONS: Anterior Q wave infarction is associated with greater transmurality and more postinfarction left ventricular remodeling and dysfunction than is non-Q wave infarction.

Animals↗

PubMed1992

Impact of increased infarct transmurality on remodeling and function during healing after anterior myocardial infarction in the dog.

To determine the impact of greater infarct transmurality on changes in left ventricular remodeling and function after acute anterior myocardial infarction, serial topographic and functional parameters (two-dimensional echocardiograms) and hemodynamics over 6 weeks, and postmortem topography (planimetry) at 6 weeks, were measured in chronically instrumented dogs randomized to standard coronary artery ligation (group 1) or a modified lower ligation plus collateral obliteration to decrease collateral inflow and increase transmurality (group 2). At 6 weeks, postmortem scar size and collagen were similar in the two groups, but group 2 had greater transmurality associated with more necrosis relative to area at risk, Q waves, infarct expansion, thinning, regional bulging, and cavity dilatation. Over the 6 weeks, group 2 showed more early expansion, late thinning and regional bulging in the short axis, larger diastolic and systolic volumes, and more apical aneurysmal bulging in the long-axis, reflecting more topographic deterioration. More important, group 2 showed greater regional and global left ventricular dysfunction over 6 weeks, lower ejection fraction at 2 days with further decrease over 6 weeks, and more left ventricular thrombus, ventricular arrhythmias, and deaths. In addition, transmurality correlated with the severity of remodeling and dysfunction. The findings indicate that transmurality is a major determinant of remodeling and left ventricular dysfunction during healing after anterior infarction.

Animals↗

PubMed1992

Effect of left ventricular unloading with captopril on remodelling and function during healing of anterior transmural myocardial infarction in the dog.

OBJECTIVE: To determine whether left ventricular (LV) unloading with captopril between two days and six weeks during healing after transmural anterior acute myocardial infarction might prevent further LV remodelling and preserve function in the canine model. DESIGN: Serial LV topographic and functional parameters (two-dimensional echocardiograms) and hemodynamics over six weeks and scar topography (planimetry) and collagen (hydroxyproline) at six weeks were measured in 34 chronically instrumented dogs; 24 with anterior transmural acute myocardial infarction (coronary artery ligation and collateral obliteration) that had been randomized at two days post infarction to therapy with oral 50 mg bid placebo (n = 12) or captopril (n = 12) for six weeks, and 10 with sham infarction. MAIN RESULTS: At six weeks, captopril and placebo groups had similar scar mass (7.7 versus 8.1% LV), infarct hydroxyproline and transmurality but the captopril group showed significantly less (P less than or equal to 0.05) infarct expansion and thinning, cavity dilation, epicardial and endocardial bulge. Between two days and six weeks, captopril decreased mean left atrial and arterial pressures compared to placebo or sham. Echocardiograms at two days showed similar LV asynergy, ejection fraction, infarct expansion and thinning with placebo and captopril. In contrast, echocardiograms between two days and six weeks showed that: further expansion and thinning occurred with placebo but not captopril; LV volumes increased with placebo but decreased with captopril; total LV asynergy was unchanged with placebo but decreased with captopril; and LV ejection fraction was unchanged with placebo but increased with captopril. At six weeks, LV ejection fraction was 10% higher (45 versus 35%, P less than 0.001) and LV aneurysm was less frequent (33 versus 100%, P less than 0.005) with captopril compared to placebo. CONCLUSIONS: Chronic LV unloading with captopril therapy during healing after canine transmural anterior acute myocardial infarction limits further remodelling, decreases aneurysm formation and improves function.

Animals↗

PubMed1991

Intravenous nitroglycerin unloading in acute myocardial infarction.

Low-dose intravenous nitroglycerin infusion can be safely administered during acute myocardial infarction to unload the left ventricle and salvage ischemic myocardium and left ventricular geometry and function. In an experimental conscious dog model, low-dose infusion titrated to decrease mean blood pressure by 10% over the first 6 hours after coronary artery ligation resulted in 51% decrease in infarct size, 54% decrease in preload, and more than 50% increase in collateral blood flow. The same benefits were seen when methoxamine was given to counteract that 10% decrease in blood pressure. Similar short-term nitroglycerin infusion also limited remodeling in the dog model. More important, no myocardial salvage was seen with excessive nitroglycerin-induced hypotension to levels less than 80 mm Hg. Clinically, prolonged low-dose nitroglycerin infusion was evaluated in a prospective, randomized, single-blinded, placebo-controlled study of 310 patients with acute infarction: 154 received nitroglycerin and 156 received placebo. Nitroglycerin was titrated to reduce mean blood pressure by 10% in normotensive patients and up to 30% in hypertensive (blood pressure greater than 140/90 mm Hg) patients, but not to less than 80 mm Hg. Nitroglycerin produced several benefits compared with placebo: (1) smaller creatine kinase infarct size; (2) less regional left ventricular dysfunction, better global ejection fraction, and less infarct expansion and thinning; (3) better clinical functional status and hemodynamics; (4) fewer inhospital complications such as acute left ventricular failure and dilation due to marked infarct expansion, left ventricular thrombus, cardiogenic shock, and infarct extension; and (5) fewer deaths up to 1 year in patients with anterior Q-wave infarction.

Animals↗

PubMed1991

Nitrates for myocardial salvage in the 1990s.

Low-dose intravenous nitroglycerin infusion for the first 48 h is becoming routine in the management of acute myocardial infarction in North America. It is most widely used as primary therapy in patients admitted more than 6 h after acute infarction. Such therapy has been shown to limit infarct size, infarct complications and remodeling. However, it is being applied increasingly more as an adjunct before, during and after thrombolytic therapy. Several trials are underway to test the effectiveness of more prolonged therapy, with early intravenous nitroglycerin followed by buccal or oral formulations for several weeks, in further limitation of ventricular remodeling, dilatation, aneurysm formation and in preserving function. Nitrates may prove to be a useful adjunct or alternative to angiotensin-converting-enzyme (ACE) inhibitors for long-term therapy.

Acute Disease↗

PubMed1990

Identification of patients prone to infarct expansion by the degree of regional shape distortion on an early two-dimensional echocardiogram after myocardial infarction.

Early detection of potential expanders (patients who develop clinically significant infarct expansion with acute left ventricular (LV) dilatation and failure but no necrosis) after acute myocardial infarction (AMI) is necessary in order to apply preventive therapy. To determine whether the degree of regional shape distortion (RSD), or dilatation, on early two-dimensional echocardiogram (2-D echo) after AMI can identify potential expanders, serial clinical and echocardiographic data were studied prospectively in 244 consecutive patients with a first Q-wave AMI. Initial (mean 2 days) and final (mean 10 days) two-dimensional echocardiograms were compared for regional LV asynergy, RSD, and conventional indices of expansion measured on endocardial diastolic outlines of mid-LV short-axis sections. Analysis of clinical and 2-D echo data revealed 51 expanders and 193 nonexpanders. Expanders showed greater LV dysfunction and more inhospital deaths (27% vs. 8%, p less than 0.001) compared with nonexpanders; conventional indices of expansion showed more marked increase between initial and final two-dimensional echo in expanders, but initial indices were not predictive. In contrast, the new RSD index Pk, a measure of the outward bulge, was markedly greater in expanders than nonexpanders on both initial (16.5 vs. 2.4 mm, p less than 0.001) and final echo. Furthermore, expanders with greater than or equal to 30% increase in Pk (to 21 mm) developed rupture of the ventricular septum (n = 10) or free wall (n = 2). Also, 50 of 51 expanders compared with 3 of 193 nonexpanders had a Pk greater than or equal to 10 mm on the initial echo. A simpler index, the depth of RSD (rd), provided similar discrimination as Pk. Thus, the degree of diastolic RSD on an early 2-D echo after AMI can identify potential expanders.

Adult↗

PubMed1989

Tolerance with low dose intravenous nitroglycerin therapy in acute myocardial infarction.

The question of vascular tolerance was examined in 154 patients with acute myocardial infarction (64 anterior, 90 inferior) who were treated with prolonged low dose intravenous nitroglycerin in a recent randomized placebo-controlled study. The dose of nitroglycerin was carefully titrated to decrease mean blood pressure by 10% in normotensive patients and 30% in hypertensive (blood pressure greater than 140/90 mm Hg) patients, but not less than 80 mm Hg. Tolerance was defined as the need to increase the dose to maintain this hemodynamic effect. It was labelled "true" if chest pain was absent and "apparent" if chest pain was present. Group analysis of dose, pain scores, hemodynamic, 2-dimensional echocardiographic and clinical parameters monitored serially before and after therapy indicated benefit with nitroglycerin over placebo despite equalizing of blood pressures after 10 hours. Reversal of blood pressures and volumes after discontinuing nitroglycerin suggested lack of significant tolerance. However, detailed individual analysis suggested significant hemodynamic tolerance in 37 patients (24%), both in the true tolerance (12%) and apparent tolerance (12%) subgroups. Tolerance appeared early, requiring the dose to be increased by 30 +/- 39 micrograms/min within 11 +/- 9 hours. The dose was greater (p less than 0.001) in the tolerance than in the no tolerance subgroup, both before (60 vs 27 micrograms/min) and after (90 vs 38 micrograms/min) 10 hours. Tolerance blunted the beneficial effect on infarct size, but positive effects on function, topography and complications persisted.

Blood Pressure↗

PubMed1989

Prospective two-dimensional echocardiographic evaluation of left ventricular thrombus and embolism after acute myocardial infarction.

To determine whether two-dimensional echocardiography can identify patients with left ventricular thrombus after myocardial infarction who are prone to embolism, clinical and echocardiographic variables in 541 patients with a first infarction between 1979 and 1983 were studied prospectively. The first echocardiogram showed definite thrombus in 115 patients (Group 1, 21%) and no thrombus in 426 (Group 2, control). In Group 1, 27 patients (23%) had clinical evidence of systemic embolism related to the thrombus before referral (Group 1a) and 88 did not (Group 1b); these two groups were similar in age, gender and infarct location, but more Group 1a patients were within 1 month of the acute infarction. In both Groups 1a and 1b, the thrombus was found in apical views over asynergic zones, with no difference (p greater than 0.05) between the two groups in the size (average area from two views being 5.3 versus 4.5 cm2), type (protruding in apical views 30% versus 27%), location (apical 83% versus 86%; septal 11% versus 11%; posterior 4% versus 2%), extent of asynergy (31% versus 33%) and ejection fraction (33% versus 34%). However, the frequency of anticoagulant therapy was less (26% versus 63%, p less than 0.005), adjacent hyperkinesia greater (100% versus 49%, p less than 0.005) and thrombus mobility greater (81% versus 19%, p less than 0.005) in Group 1a than in Group 1b. Serial echocardiograms revealed a decreased size of the thrombus by 6 months in both Groups 1a and 1b, and little or no trace in 85% by 24 months. Thus, ventricular thrombus size, location and protrusion in apical views on echocardiography did not correlate with embolism. In contrast, thrombus mobility, the presence of adjacent hyperkinesia and thrombus protrusion assessed in multiple views appeared to be strong discriminators of thrombus prone to embolism. These echocardiographic features might provide a guide for the duration of anticoagulant therapy.

Adult↗

PubMed1989

Nitroglycerin in acute myocardial infarction.

Nitroglycerin is an effective agent for reducing preload and afterload in acute myocardial infarction. Until two decades ago, it was considered to be contra-indicated in acute myocardial infarction because of fear of hypotension and reflex tachycardia. Recent animal studies indicated that prolonged low dose infusion during early stages of acute infarction, titrated to decrease mean arterial pressure by 10% but not below 80 mmHg, produced marked increase in collateral blood flow and decrease in infarct size. However, higher doses to further decrease blood pressure offset the beneficial effect on collateral flow and infarct size. More importantly, clinical studies have confirmed that low dose intravenous nitroglycerin is safe therapy during acute myocardial infarction for improving left ventricular performance, limiting infarct size and reducing infarct related complications.

Animals↗

PubMed1989

Nitrates in acute myocardial infarction--state of the art.

Until the 1970s, nitroglycerin was used mainly for controlling angina pectoris. It was generally avoided in the setting of acute myocardial infarction. The main reason was fear of hypotension and reflex tachycardia. Experimental and clinical data since the mid-1970s indicate that hypotension should indeed be avoided during acute infarction. More important, prolonged low-dose intravenous nitroglycerin is now regarded as safe therapy during acute infarction for improving left ventricular performance, limiting infarct size, and reducing infarct-related complications.

Dose-Response Relationship, Drug↗

PubMed1989

Improved left ventricular function and topography by prolonged nitroglycerin therapy after acute myocardial infarction.

To determine whether decreasing preload and afterload by prolonged nitroglycerin therapy (NTG) after acute myocardial infarction (AMI) might improve left ventricular (LV) geometry and function, 43 patients with a first anterior transmural AMI (ATAMI) were given low-dose intravenous NTG infusion for the first 48 h and then randomized to buccal NTG (1-3 mg t.i.d., five hourly with an eight-h washout period to avoid vascular tolerance; dose titrated as for i.v. NTG for 10% decrease in blood pressure but not below 80 mm Hg) or placebo for six weeks. All patients had serial two-dimensional echocardiography for 12 weeks for regional LV function and topography: Expansion index = asynergic/non-asynergic endocardial segment length; Thinning ratio = asynergic/normal wall thickness. Asynergy was defined as akinesis + dyskinesis. Between initial and 12-week studies, expansion index did not change in the buccal NTG group (2.09 vs 2.28, N.S.; n = 23) but increased in the placebo group (2.10 vs 2.89, p less than 0.05; n = 20). Over the same period, thinning ratio was unchanged with buccal NTG (0.82 vs 0.77, N.S.) but increased with placebo (0.78 vs 0.66 p less than 0.05). Both expansion and thinning at 12 weeks were greater with placebo than buccal NTG (p less than 0.01). The results indicate that prolonged NTG therapy decreased infarct expansion and infarct thinning. Compared to placebo, the NTG group also showed improved hemodynamics, decreased LV volume and asynergy, and increased ejection fraction. Thus, prolonged NTG therapy after ATAMI preserves LV function and topography. The beneficial early and late remodeling with prolonged NTG therapy might prevent aneurysm formation.

Administration, Buccal↗

PubMed1989

Myocardial infarct expansion during indomethacin or ibuprofen therapy for symptomatic post infarction pericarditis. Influence of other pharmacologic agents during early remodelling.

Evidence of acute infarct expansion and the frequency of the acute infarct expansion syndrome (acute infarct dilatation and thinning associated with hypotension and left ventricular failure but no evidence of new necrosis) occurring at two days or more after a first acute Q-wave myocardial infarction were studied using serial two-dimensional echocardiography in 221 consecutive patients (100 anterior, 121 inferior). Patients with symptomatic pericarditis were treated with indomethacin (group 1, n = 73) or ibuprofen (group 2, n = 49) and those without symptomatic pericarditis received neither drug (group 3, n = 99). The overall frequency of the acute infarct expansion syndrome was 13% and 69% of these were among the pericarditis groups. The syndrome was significantly more frequent in group 1 (22%) than group 2 (8%) (P less than 0.05) or group 3 (9%) (P less than 0.025). Serial echocardiograms revealed more expansion with greater percentage increase in the infarct containing segment length in group 1 than group 2 or group 3 (18% versus 9% versus 9%, P less than 0.005). However, the decreases in infarct segment thickness were similar in groups 1 (24%) and 2 (25%) but greater (P less than 0.001) than in group 3 (7%). Despite similar infarct size and infarct thinning in groups 1 and 2, the degree of infarct expansion was greater and the infarct expansion syndrome more frequent in group 1. However, when allowance was made for the potential protective effect of prior use of intravenous nitroglycerin and concomitant use of nifedipine, indomethacin and ibuprofen had similar effects on expansion. Thus, indomethacin or ibuprofen should be used with caution after Q-wave infarction so as to avoid further expansion. The fact that short term use of other drugs might modify infarct remodelling should be considered in studies attempting to assess efficacy of one particular drug.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Antagonists↗

PubMed1988

Exercise training after anterior Q wave myocardial infarction: importance of regional left ventricular function and topography.

To determine whether the extent of left ventricular dysfunction and the degree of shape distortion can predict outcome in survivors of moderate-sized anterior Q wave myocardial infarction who are undergoing exercise training, these variables were measured by two-dimensional echocardiography before and after 12 weeks of a low level exercise training program starting 15 weeks after infarction in 13 patients (7 in group 1 and 6 in group 2) and 12 weeks apart in 24 matched control patients without training. By the end of training, the functional class score had increased in group 2 (from 2.25 to 2.67, p less than 0.005) but had not changed in group 1. Further discrimination of groups 1 and 2 was provided by an initial asynergy (akinesia or dyskinesia, or both) less than 18% or greater than or equal to 18%. Compared with group 1, group 2 had greater initial asynergy (32 versus 6%, p less than 0.001), expansion index (asynergic/normal endocardial segment length: 1.8 versus 1.6, p less than 0.025) and peak shape distortion index (12.2 versus 1.0 mm, p less than 0.005) but lower ejection fraction (43 versus 59%, p less than 0.05) and thinning ratio (asynergic/normal wall thickness: 0.61 versus 0.74, p less than 0.05). These variables did not change with training in group 1. However, in group 2, training caused significant increase in asynergy (from 32 to 40%, p less than 0.05), expansion index (from 1.8 to 2.0, p less than 0.01) and peak shape distortion (from 12.2 to 20.9 mm, p less than 0.05) associated with a decrease in thinning ratio (from 0.61 to 0.51, p less than 0.001) and ejection fraction (from 43 to 30%, p less than 0.005). Initial values for these variables were similar for corresponding control groups but did not change over the 12 weeks. Thus, patients with greater than or equal to 18% left ventricular asynergy on the initial echocardiogram showed more shape distortion, expansion and thinning before exercise training and developed further functional and topographic deterioration with training.

Adult↗