Previous Transmural Myocardial Infarction Research Articles

Post myocardial infarction left ventricular dysfunction – Assessment and follow up of patients undergoing surgical ventricular restoration by the endoventricular patchplasty

Authors of this important article by D'Mello et al, have nicely presented a prospective study of clinical and echocardiographic follow up of Left Ventricular (LV) geometry of 59 consecutive patients with previous transmural anterior myocardial infarction, who underwent LV restoration, analyzed between June 2007 and May 2008.1 The authors are to be complemented for this important series which showed excellent immediate and short-term results following LV restoration surgery. The results show a progressive remodeling after ventricular reconstruction mainly by excluding the scar area. Volume reduction is more important than the post surgical shape of the ventricle. The study was done before the MRI era; and hence the images of the scar are not demonstrated in the study.2,3 Analysis of the precise mechanism of remodeling is perhaps not possible without MRI. Distinction between dyskinetic and akinetic forms of the scar are not clearly brought out; it is usually transmural with dyskinesia and subendocardial with akinesia. The size of a synergy and its extension determine the extent of remodeling.4,5 It is surprising that these 59 patients were not severe cases of ischemic failing ventricle, as the mean ejection fraction was 33.5 ± 5%, preoperative end diastolic volume index 89.7 ± 6 and end systolic volume index 48.8 ± 11.3 which are below the threshold of very severe cardiac failure. White et al have given a figure of >60 ml of end systolic volume index as the major determinant of survival after recovery from myocardial infarction.6 This work is indeed of great interest and I hope the authors with their experience will present more severe cases showing a positive interest in LV reconstruction and thereby demonstrating that the S.T.I.C.H trial was a miss organized trial.7 The global approach of heart failure by Buckberg cannot be accepted; it is apparent that Buckberg is a prisoner of his “flying fancies” trying to establish something without any serious base.7 The myocardial systolic contraction is a “twist up” like a “snake” ascension. The crux of the problem of systolic heart failure is the ventricular spherical dilatation whatever be the anatomic substrate. The surgical ventricular restoration (S.V.R) or surgical anterior ventricular restoration (S.A.V.R) are acronyms in place of left ventricular reconstruction (L.V.R.) because this technique is applied most of time only for anterior LV wall, with the objective of “volume reduction” and to get an elliptical shape of LV. Finally, I would like to emphasize the following points: Ventricular wall has a systolic concentric (centripetal contraction) confirmed by MRI video examination of left ventricular wall in 4 projections.8 Heart failure is not an entity but a syndrome with various causes; in post myocardial infarction failure, the cause is an extension of the necrotic, then fibrous and finally calcified transmural or subendocardial scar, when it reaches = or <30% of LV perimeter. The dilatation is not the cause, but the consequence; dilatation is more ovoid than spherical. LVR as proposed by as in 1984, have these main goals: to suppress or exclude the scarred asynergic wall, to abolish the mechanism of progressive dilatation i.e. the eccentric systolic motion, restoring the curvature of non-infarcted myocardium and maintain the physiological diastolic volume of the rebuilt cavity by balloon sizing before “clothing” of the cavity by a patch anchored on contractile edge of normal myocardium.9 In conclusion, this article by D'Mello et al demonstrates and emphasizes the modern approach toward post myocardial infarction heart failure which is a very prevalent disease encountered in day to day clinical practice.

A 32‐year‐old woman with arthralgias and severe hypotension

A 32‐year‐old woman with arthralgias and severe hypotension

Section 10: Surgical Approaches to the Treatment of Heart Failure

Section 10: Surgical Approaches to the Treatment of Heart Failure

Significance of systolic anterior motion of the mitral valve during dobutamine stress echocardiography

Left ventricular outflow tract obstruction related to systolic anterior motion of the mitral valve (SAM) induced during dobutamine stress echocardiography (DSE) is not unusual but its significance is not established. A total of 100 consecutive patients (mean age 62 +/- 12 years; 67% male) without previous transmural myocardial infarction, valvular disease, or hypertrophic cardiomyopathy, undergoing DSE to assess the presence of myocardial ischemia, were prospectively evaluated. A SAM with DSE was searched and correlated with clinical and baseline echocardiographic findings. Patients who demonstrated SAM with DSE were selected for exercise echocardiographic Doppler study with bicycle, within 6 months of the DSE. The development of an intraventricular gradient with DSE or exercise was defined as a new gradient of > or =36 mm Hg. In all, 23 patients developed SAM during DSE with a mean gradient of 79 +/- 33 mm Hg (range: 39-144 mm Hg) and mitral regurgitation related to SAM. Compared with patients without SAM, patients who developed SAM with DSE were characterized at rest by a smaller mitroaortic angle and septoaortic angle, a higher posterior mitral leaflet length, and a smaller left ventricular cavity. Neither ischemic nor hypotensive response during DSE were correlated to SAM. In the group of patients with SAM, of the 9 patients who were referred for unexplained chest pain or dyspnea, 5 reproduced symptoms with DSE, compared with 2 of 17 patients in the group without SAM (P = .005). Despite these findings, only 3 of the 16 patients who underwent exercise echocardiography Doppler study developed SAM (two with symptoms), with a wide range of achieved heart rate, compared with DSE. Although patients with SAM with DSE exhibit predisposing echocardiographic findings, the clinical impact of this phenomenon is real in only a minority of patients, particularly those who experienced unexplained dyspnea or chest pain.

Homocysteine Plasma Levels in Young Patients with Coronary Artery Disease: Relation to History of Acute Myocardial Infarction and Anatomical Extent of Disease

Although there is considerable epidemiologic evidence for a relationship between plasma homocysteine (Hcy) levels and cardiovascular disease, not all prospective studies have shown such a relationship. Furthermore, data concerning the role of hyperhomocysteinemia in patients with premature coronary artery disease (CAD) are rare. It was the aim of the study to investigate a possible association between Hcy plasma levels in young patients with the extent of CAD and the history of myocardial infarction (MI). A cohort of 94 patients was examined for conventional risk factors and the history of previous transmural MI. Furthermore, coronary angiography was performed to assess the anatomical extent of vessel disease. Plasma Hcy levels were measured by use of a commercial enzyme-linked immunosorbent assay. Only a history of previous MI was significantly associated with hyperhomocysteinemia. There was no relationship between elevated Hcy levels and the anatomical extent of vessel disease in patients with premature CAD. Our data may indicate that hyperhomocysteinemia represents an independent risk factor for acute coronary thrombosis rather than for the development of coronary sclerosis. Thereby, hyperhomocysteinemia may influence the clinical situation after plaque rupture not only by prothrombotic action but also by favouring endothelial dysfunction and vasospasm.

Myocardial flow reserve parametric map, assessed by first-pass MRI compartmental analysis at the chronic stage of infarction.

Regional myocardial flow and flow reserve (MFR) were assessed by compartmental analysis of Gd-enhanced MRI first-pass data in 7 patients with atypical chest pain, and in 15 patients with previous transmural myocardial infarction. The FE product (Flow x Extraction coefficient), derived from the modified Kety equation, was measured in regions corresponding to the Tetrofosmine-SPECT fixed defect and in remote normal regions. The FE product at rest and hyperemic FE product were similar in healed revascularized tissues (70.5 +/- 15.6 and 112.5 +/- 19.5 ml/mn/100 g, respectively) and in normal myocardium (76.2 +/- 18.3 and 142.2 +/- 33.0, respectively). In contrast, the FE index (48.8 +/- 15.2 and 60.7 +/- 18.0, respectively, P < 0.01 versus the two previous groups) and the MFR (1.27 +/- 0.20 vs. 1.91 +/- 0.29 in normal regions) were reduced in healed fibrotic tissues when the infarct-related artery remained occluded. Myocardial flow reserve maps allowed correct identification of regions corresponding to an occluded infarct-related artery.

Effects of the Dor procedure on left ventricular dimension and shape and geometric correlates of mitral regurgitation one year after surgery

Objectives: In the present study we retrospectively analyzed ventriculographic data from symptomatic patients after myocardial infarction who underwent the Dor procedure (endoventricular circular patch plasty repair) to evaluate left ventricular shape 1 year after the operation and to analyze the geometric correlates of late mitral regurgitation. Methods: Forty-four patients with previous transmural anterior myocardial infarction comprised the study group. Left ventricular volumes, global left ventricular systolic and diastolic sphericity, the extent of wall motion abnormalities, and the presence and degree of mitral regurgitation were analyzed before and 1 year after operation. Results: Comparing preoperative diastole to systole within the cardiac cycle, left ventricular shape becomes more elliptical in systole than it was in diastole (eccentricity index closer to 1). The intervention leads to an increased diastolic sphericity, but for each cardiac cycle, the systolic shape is more elliptical relative to its diastolic counterpart in respect to basal conditions. Mitral regurgitation was detected after operations in 17 patients; 14 of them did not have mitral regurgitation before operations. Patients with late mitral regurgitation had greater preoperative volumes and more spherical chamber than did patients without late mitral regurgitation. Conclusions: Despite a more spherical postoperative left ventricular chamber, systolic pump function improves after the Dor procedure, mainly for the improvement in inferior wall shortening. The presence of late mitral regurgitation is relatively frequent in this series of patients, and this emphasizes the importance of a more accurate quantitative evaluation of preoperative functional mitral regurgitation to repair the valve when appropriate. Geometric correlates of late mitral regurgitation appeared to be greater chamber sphericity and larger ventricular volumes preoperatively. (J Thorac Cardiovasc Surg 2001;121:91-6)

Modification in serum concentrations of aminoterminal propeptide of type III procollagen in patients with previous transmural myocardial infarction

The aim of our study was to evaluate the modification of serum concentration of aminoterminal propeptide of type III procollagen (PIIINP) in 70 patients with previous transmural myocardial infarction. In 38 patients (group 1) PIIINP levels increased at 6 and 12 months after infarction; in 32 patients (group 2) PIIINP increased at 6 months, returning to baseline at 12 months. At the same time we observed a significant left ventricular enlargement and worsening of the performance in group 1, whereas in group 2 an improvement was seen in left ventricular volumes and performance. In conclusion, rearrangement of collagen myocardial matrix plays an important role in left ventricular postinfarction modification. This process can be easily followed over time in a noninvasive manner by dosing serum PIIINP concentrations. (Am Heart J 1998;135:287-92.)

Left ventricular filling rate at rest and during exercise in patients with previous myocardial infarction

The purpose of this investigation was to define, with radionuclide technique, the variation on left ventricular filling rate in patients with coronary artery disease, and to determine the effects of dynamic exercise on this variation. The study was carried out on 91 subjects, 46 patients with anterior and 30 with inferior previous transmural myocardial infarction; 15 healthy subjects were studied as control group. All the patients underwent coronary angiography and left ventriculography. From the left ventricular time activity curve we considered the diastolic parameters of the peak filling rate (PFR). We considered also the relative end-diastolic volume (rEDV) and the relative end-systolic volume (rESV). These parameters were determined at rest and at the fifth minute of a symptom limited dynamic exercise taken in the supine position, on an ergometric bicycle. In normal subjects rest mean PFR values is 3.08 ± 0.51 edv/s, during exercise occurs a physiological increase and mean PFR values becomes 5.48 ± 1 edv/s. The patients with previous myocardial infarction show a PFR significantly smaller than in normal subjects. Abnormal PFR indices during exercise are present in a large number of these patients and the higher anomalies of PFR during exercise were found among patients with anterior myocardial infarction. In these patients we found an increase of rESV during exercise. In conclusion myocardial infarction induces significant alterations of the PFR; physical exercise reveals PFR alterations not exhibited at rest and rESV increase during exercise could be responsible for the PFR alteration observed.

Success and complication rates of coronary angioplasty in patients with and without previous myocardial infarction

The primary success rate and incidence of major complications have been retrospectively assessed in a consecutive series of 224 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) in one centre. The patients have been divided into three groups; those with angina and no previous myocardial infarction (Group 1; N = 130), those with angina and a previous transmural myocardial infarction (TMI) (Group 2; N = 59), and those with angina and a previous non-transmural myocardial infarction (NTMI) (Group 3; N = 26). The three groups were well matched for age, gender and angiographic severity of stenosis. The primary success rate in Group 1 was 90% compared to 64% in Group 2. The success rate in Group 3 lay in between at 77%. The lower success rates in Groups 2 and 3 were mainly due to an increase in the frequency of major complications. Acute coronary occlusion occurred in seven patients in Group 1, nine patients in Group 2 and four patients in Group 3. In all these patients in Groups 2 and 3 the outcome of acute occlusion was a procedure-related clinical myocardial infarction despite immediate re-angioplasty and/or emergency coronary artery bypass grafting whereas only four patients in Group 1 sustained an acute infarct. In this series of patients undergoing coronary angioplasty for symptom limiting angina, previous myocardial infarction appears to be a risk factor for a lower success rate mainly due to an increase in the frequency and severity of major complications.

Value of exercise electrocardiography to predict additional jeopardized myocardial regions remote from site of previous myocardial infarction.

In order to evaluate the efficacy of exercise electrocardiography (ECG) to identify jeopardized myocardial regions remote from the site of previous infarction, exercise ECG, left ventriculography, and coronary arteriography were performed in 90 patients with previous transmural myocardial infarction (MI). Of the 90 patients, angiographic studies revealed jeopardized myocardial regions in 47 patients. Exercise ECG correctly identified 32 of these 47 patients for a sensitivity value of 68%. There were 43 patients without any additional jeopardized myocardial regions. Exercise ECG correctly identified only 24 of these 43 patients for a specificity value of 56%. The sensitivity and specificity values were similar in patients with prior anterior and inferior wall MI. It is concluded that relatively low sensitivity and specificity values preclude the ability of exercise ECG to accurately identify patients with jeopardized myocardial regions distant from the site of previous MI. Moreover, when such patients were correctly detected, exercise ECG was rather poor in localizing these additional jeopardized myocardial areas.

Correlations of systolic time intervals and radionuclide angiography at rest and during exercise

Systolic time intervals (STI) were correlated with radionuclide angiography studies (RAS) in 57 patients at rest, during maximal semisitting bicycle exercise, and at 4 minutes following the cessation of exercise. Eleven were judged as being free of coronary artery disease (group 1), while 14 had coronary artery disease without (group 2A), and 27 (group 2B) with a previous transmural myocardial infarction. For RAS, resting radionuclide ejection fraction (REF), the changes in REF and end-systolic volume, and the development of a wall motion abnormality at peak exercise were each highly correlated with the presence of coronary disease ( p < 0.001). The accuracy of STI parameters in predicting the presence of coronary disease was poor (<60%). Changes in end-diastolic volume (EDV) correlated significantly with PEP LVET and LVET, changes following exercise. Moreover, patients with an abnormal (>25%) increase in EDV at peak exercise had a greater increase in LVET, in the postexercise period ( p < 0.01). We conclude that STI is not accurate enough a predictor of coronary disease or left ventricular function to serve as a useful screening test. Changes in STI parameters appear to be more related to changes in ventricular volume than to ventricular function.

Left ventricular function and extent of coronary artery disease in the absence of antecedent myocardial infarction in patients with ischemic cardiac pain.

Left ventricular (LV) function and extent of coronary artery disease (CAD) are important prognostic factors in patients with ischemic cardiac pain (ICP). This study was designed to compare LV function in patients with ICP admitted to our coronary care unit (CCU). Patients with previous transmural myocardial infarction (TMI) or who were over age 75 were excluded. Group 1 (n = 17) developed their 1st TMI; group 2 (n = 14) were diagnosed as unstable angina (UA). All patients demonstrated significant CAD on arteriography; i.e., at least 70% stenosis of at least 1 major coronary vessel. LV function was evaluated by single plane ejection fraction (EF), end-diastolic volume index (EDVI) (ml/m2), and the slope of a modified LV function curve (S) utilizing change in CI divided by change in end-diastolic pressure at rest and post-LV angio (ml X min X M-2 X mm Hg) (normal +/- SD: 176 +/- 39). Both TMI and UA patients had LV dysfunction; although group 1 had more severe abnormalities, they were not statistically significant. Eleven (65%) in group 1 and 10 (71%) of 14 in group 2 had multivessel CAD. We conclude that in patients without previous TMI admitted with ICP: (1) Those who do not develop TMI have similar LV dysfunction compared to those with TMI; and (2) TMI and UA patients have similar multivessel CAD.

Early repair of ventricular septal rupture after infarction

The cases of 27 consecutive patients aged 40 to 78 years with ventricular septal rupture during acute myocardial infarction were reviewed. Myocardial infarction was inferior in 16 patients and anterior in 11. The time from myocardial infarction to rupture was less than 24 hours in 9 patients, 24 to 48 hours in 6 patients, 2 to 7 days in 11 patients, and 14 days in 1 patient. In 23 patients pressures (in mm Hg) were pulmonary arterial systolic 28 to 70 (mean 52), diastolic 9 to 34 (mean 23) and left ventricular end-diastolic 15 to 35 (mean 24). Cardiac index was 1.1 to 2.5 (mean 2.0) liters/min per m 2 and the ratio of pulmonary to systemic flow ( Q p Q s ) 1.5 to 4.8 (mean 3.4). The number of coronary vessels with more than 50 percent obstruction was one in 8 patients, two in 11 patients and three or more in 8 patients. Of the eight patients with single vessel disease three had right, one had left circumflex, and four had left anterior descending coronary artery disease. All seven patients treated without surgery died 1 to 13 days after ventricular septal rupture; all seven had inferior myocardial infarction, and none had previous transmural myocardial infarction. Of these seven patients, two were considered inoperable, one died during study, and four died abruptly while awaiting study. Eleven of 20 patients (55 percent) survived operation. The survival rate in seven patients operated on less than 2 days after ventricular septal rupture was 72 percent. Of 11 patients operated on 2 to 28 days after ventricular septal rupture 4 survived, whereas the 2 patients operated on later than 4 weeks after rupture survived. It is concluded that (1) early surgery in ventricular septal rupture has relatively low mortality; (2) delay of study and surgery is done at the expense of unacceptable and unpredictable mortality; and (3) ventricular septal rupture can occur with single vessel coronary artery disease.

Effects of morphine on left ventricular dimensions and function in patients with previous myocardial infarction.

To assess the effects of morphine sulfate on left ventricular function and dimensions we administered 15 mg of this agent to 11 stable patients with previous transmural myocardial infarction. All studies were carried out in the supine position. Before morphine administration an echocardiogram was obtained, and this procedure was repeated at 15, 30, 60, 120, and 240 min after morphine. Heart rate decreased from a control value of 69 +/- 4 to 62 +/- 5 beats/min 2 h after morphine (p less than 0.01, analysis of variance); this slower heart rate persisted for 4 h after morphine. Serial measurements of blood pressure, echocardiographic ejection fraction, percent of fractional shortening, and mean normalized velocity of circumferential fiber shortening also showed no significant alterations after morphine. We conclude that in stable patients with chronic ischemic heart disease studied in the supine position, 1) morphine exerts no effect on left ventricular dimensions, an observation which does not support the concept that this agent acts in humans by producing a 'pharmacologic phlebotomy'; and 2) morphine does not alter left ventricular function at rest. Whether different results will be found in patients with increased sympathetic activity, such as occurs in the setting of an acute myocardial infarction or during an episode of acute pulmonary edema, remains to be investigated.

Angina, aortic stenosis and coronary heart disease.

The pre-operative clinical and haemodynamic findings of 139 consecutive patients with aortic stenosis were analysed in an attempt to determine the incidence and influence of coronary heart disease on the mode of presentation of patients with aortic stenosis. The overall incidence of coronary heart disease was 32%. 105 patients (76%) presented with angina and of these, 41 patients (39%) had significant coronary heart disease as compared to 4 (13%) of the remaining 34 patients who did not present with angina. Clinical parameters including age, sex, severity of angina together with the presence of associated symptoms and precipitating factors were unhelpful in distinguishing those patients with coronary heart disease. Evidence of previous transmural myocardial infarction or the presence of ST-T abnormalities in the absence of digitalis and the changes of left ventricular hypertrophy were reliable electrocardiographic signs of coronary heart disease. Although peak systolic aortic valve gradient tended to decrease with increasing severity of coronary heart disease, the severity of aortic stenosis was not a reliable indicator of the presence of coronary disease. Patients with coronary heart disease in the absence of angina all had a combination of moderate aortic stenosis and single vessel disease. It is concluded that coronary heart disease cannot be predicted in patients with angina and, in the absence of angina occurs with an incidence sufficiently high to advocate the use of coronary angiography as part of the investigation of all patients with aortic stenosis being considered for valve replacement.

Causes of Transient Cerebral Ischemia

To the Editor.— In editorially discussing mitral valve prolapse as another cause of cerebral ischemia (236:2783, 1976), transient or otherwise, Hussey mentioned other causes, such as bacterial endocarditis, marantic endocarditis, and mitral valve stenosis complicated by atrial fibrillation. An additional major differential diagnostic consideration was omitted, namely, cerebral embolism originating at variable intervals from a previous left ventricular transmural myocardial infarction (196:133, 1966).

Hemodynamics at Rest and during Exercise in 222 Patients with Coronary Heart Disease before and after Aorto-Coronary Bypass Surgery

In 222 patients with coronary heart disease hemodynamics at rest and during exercise were measured before and after aortocoronary bypass surgery. A total of 552 grafts were constructed, i.e. an average of 2.47 grafts per patient. Only 10.8% of the patients had a 1-vessel-disease, 59.2% had a 3-vessel-disease. 10.8% of the patients were provided with one graft, 49.7% got 3 or 4 grafts. In 92.8% of the patients the r. desc. ant. was significantly stenosed, and in 94.2% this vessel has been provided with a graft. Preoperatively only 7 patients had no angina pectoris during exercise (bicycle ergometer in supine position, each load lasting 6 min), postoperatively 154 patients have been completely free of angina pectoris. The preoperative angina pectoris-free exercise tolerance was 27.4 +/- 27.4 W (means +/- SD), postoperatively it was 76.5 +/- 33.8 W. The largest increase of exercise tolerance was observed in patients with a 3-vessel-disease (208%). Preoperatively only 10.1% had normal values of pulmonary wedge pressure and cardiac output at rest and during exercise, postooperatively 51.5%. The postoperative normalization of hemodynamics depends on the number of vessels involved (1-vessel-disease 86%, 3-vessel-disease 39.8% normalization) and on the status of the left ventricle (without a previous transmural myocardial infarction 68.4%; with a previous myocardial infarction 41.0%). The effects of revascularization on myocardial ischemia can be evaluated by measurements of pulmonary wedge pressure and cardiac output at rest and during exercise.

The natural history of trifascicular disease following permanent pacemaker implantation. Significance of continuing changes in atrioventricular conduction.

Seventy-two patients with trifasicular disease were followed for an average of 40 months following permanent pacemaker insertion. The indications for pacemaker insertion were either electrocardiographic evidence of complete heart block with a wide QRS escape complex or a pattern of bifasicular block with either periods of Mobitz type II atrioventricular (A-V) block or a documented history of syncope. The patients were then divided into three groups depending on subsequent change in A-V conduction. There were 31 (43%) patients with no change in A-V conduction, 17 (24%) with increasing A-V block, and 24 (33%) with decreasing A-V block. The characteristics of these three groups, including age and sex distribution, were compared and found to be similar. The incidence of previous transmural myocardial infarction as determined by electrocardiographic criteria was higher in the group with decreasing block. Survival curves showed a significantly decreased probablity of surviving for those with decreasing block compared to both those with increasing block and those with no charge in conduction (P less than 0.03). We conclude that the probability of long-term survival was less in the group with decreasing block. This finding may be related to the greater prevalence of coronary heart disease in the patients.

Beneficial effects of nitroglycerin on abnormal ventricular wall motion at rest and during exercise in patients with previous myocardial infarction

The effects of sublingually administered nitroglycerin on segmental left ventricular wall motion determined by videotracking and radiographic left heart size were evaluated at rest and during submaximal handgrip exercise in 10 patients with previous transmural myocardial infarction. After nitroglycerin, diastolic left heart size decreased in the resting state from an average of 49.5 ± 5.7 (standard deviation) to 47.9 ± 5.6 mm/m 2 body surface area ( P < 0.01) and during handgrip exercise from a mean of 50.7 ± 5.0 to 49.1 ± 4.7 mm/m 2 ( P < 0.05). In the resting state, the average maximal velocity of shortening in segments with normal wall motion increased after nitroglycerin from 18.1 ± 3.0 to 23.5 ± 5.5 mm/sec ( P < 0.01), whereas during handgrip exercise alone, the velocity of shortening averaged 25.6 ± 6.9 mm/sec and increased further after nitroglycerin to 30.1 ± 10.6 mm/sec ( P < 0.05). The effects of nitroglycerin on the average extent of shortening in normal segments were similar. In all 10 patients, there was a decrease-in the number of segments with abnormal wall motion. The number of sites with dyssynergy decreased after nitroglycerin from 24 to 15 in the resting state and from 40 to 22 when nitroglycerin was administered before handgrip exercise. Sublingually administered nitroglycerin appears to decrease left heart size, increase the velocity and extent of shortening in normal left ventricular segments and often reduce the extent of left ventricular wall motion abnormalities at rest and during isometric exercise in patients with previous transmural myocardial infarction.