Effects of submaximal isometric handgrip on left ventricular size and wall motion

To evaluate the effects of sustained submaximal isometric handgrip exercise on the left ventricle in patients with previous myocardial infarction, we utilized the noninvasive techniques of radarkymographic video tracking, measurement of the left heart dimension and calculation of systolic time intervals to assess alterations in wall motion and left ventricular size and function during handgrip exercise performed at a tension level of 15 percent of maximal voluntary contraction. In 9 of 12 patients with dyskinesis or asynchrony at rest the mean amplitude and velocity of systolic outward movement increased during handgrip exercise (P < 0.05), whereas in 11 patients with initially hypokinetic areas mean amplitude and velocity decreased (P < 0.05); in 3 patients dyskinesis was produced de novo. In all 12 patients both amplitude and velocity decreased in areas of normal wall motion (P < 0.05); similar changes occurred in 5 normal control subjects. Alterations in systolic time intervals during handgrip exercise were variable, and no consistent patterns were observed in either patients or control subjects. In seven patients whose left heart dimension increased during handgrip exercise, wall motion abnormalities were more severe at rest than in the five patients whose left heart dimension decreased. The five control subjects showed a decrease in left heart dimension during handgrip exercise.We conclude that the normal response to submaximal isometric handgrip exercise at 15 percent of maximal voluntary capacity is a decrease in left ventricular size and a reduction in both the amplitude and velocity of left ventricular wall motion. Furthermore, in patients with previous myocardial infarction sustained isometric handgrip exercise is a useful maneuver for the intensification or induction of left ventricular wall motion abnormalities. By contrast, no consistent alterations in systolic time intervals were observed during handgrip exercise either in normal subjects or in patients with previous myocardial infarction. Thus, systolic time intervals do not appear to be useful for evaluating the left ventricular response to submaximal handgrip exercise in individual patients.     

The isovolumic index: A new noninvasive approach to the assessment of left ventricular function in man

Both a high ratio of preejection period (PEP) to left ventricular ejection time (LVET) and a prolonged isovolumic relaxation time are associated with left ventricular dysfunction. In pilot studies in instrumented dogs, we measured a combined isovolumic index, defined as (isovolumic contraction + isovolumic relaxation time)/LVET and found an inverse correlation with changes in fractional shortening. To test the utility of this index in human subjects, we used the electrocardiogram, mitral valve (MV) echogram, and indirect carotid arterial tracing to calculate isovolumic index as (time from R wave to MV opening — LVET)/LVET × 100%. Normal subjects had isovolumic index values that averaged 24 ± 7% (standard deviation), in contrast to patients with cardiomyopathy who averaged 5 ±14% (p < 0.001 versus normal values) and patients with coronary artery disease who averaged 40 ±15% (p < 0.001 versus normal values and patients with cardiomyopathy). All normal subjects had an isovolumic index of < 32% and all patients with cardiomyopathy had values >32%. Of patients with coronary artery disease, 72% (21 of 29) had an isovolumic index >32%. An isovolumic index >32% identified 20 of 22 patients (91%) with a reduced ejection fraction and 12 of 14 (86% ) with a segmental wall motion abnormality, and it was a more sensitive marker of these abnormalities than abnormal E point-septal separation. In 6 patients with coronary artery disease who had simultaneous echocardiograms and measurements of left ventricular pressure by micromanometer tip catheter, the time constants of isovolumic pressure decrease were uniformly increased in association with an isovolumic index >32%. In contrast, all had normal PEP/LVET ratios. The isovolumic index is thus a sensitive, potentially useful noninvasive marker of left ventricular dysfunction that is easily obtained from the routine echocardiogram.     

Beneficial effects of nitroglycerin on abnormal ventricular wall motion at rest and during exercise in patient 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 hand grip 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/m2 body surface area (P less than 0.01) and during handgrip exercise from a mean of 50.7 +/- 590 to 49.1 +/- 4.7 mm/m2 (P less than 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 less than 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 less than 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.     

Echocardiographic evaluation of left ventricular function in children with congestive cardiomyopathy

Echocardiography was used to study left ventricular function in 37 children with congestive cardiomyopathy. Left atrial and left ventricular diameters were approximately 1.5 times that predicted by body weight, whereas systolic decrease in left ventricular diameter (shortening fraction) and increase in posterior wall thickness were half that of normal children. The ratio of left ventricular preejection period to ejection time was increased in 25 patients and normal in 10. The mean velocity of circumferential fiber shortening was decreased in 30 of 34 patients and averaged 52 percent of that predicted by heart rate.

The shortening fraction was higher in the 12 patients who were asymptomatic at the time of study than in the 25 who had symptoms of congestive heart failure (19.6 ± 2.4 standard error of the mean versus 14.6 ± 1.2) (P < 0.05). In 11 patients whose condition improved after therapy with digoxin and diuretic drugs, serial echocardiograms showed significant increases in shortening fraction and posterior wall thickening and decreases in left atrial diameter and the ratio of preejection period to ejection time. However, one or more indexes of left ventricular function remained abnormal, despite the resolution of symptoms and a return of heart size to normal as judged from the chest roentgenogram.     

Normal angiogram after myocardial infarction in young patients:: A prospective clinical-angiographic and long-term follow-up study

This is an observational study in which we compared the clinical characteristics and the long-term course of young patients having acute myocardial infarction and angiographically normal coronary arteries and young patients showing significant coronary artery disease. In 87 patients aged ≤40 years who suffered an acute myocardial infarction, enrolled in a prospective study over a period of 6.5 years, coronary anatomy was determined by angiography within a month of admission. The risk factors, clinical data, ventricular function and the long-term outcome were compared between patients with normal angiograms (Group 1, n=12) and patients with coronary artery disease (Group 2, n=75). Patients in Group 1 had a lower number of risk factors associated with them (17% vs. 64% with >1 risk factor, P<0.005), were younger (32±5 vs. 36±4, P<0.01), lighter smokers (25% vs. 55% for ≥2 packs per day, P<0.05), had less frequent hypertension (0 vs. 25%, P<0.05), hypercholesterolemia (17% vs. 52%, P=0.02) and had a lower mean total cholesterol level (201±42 vs. 245±60 mg/100 ml, P<0.05) than patients in Group 2. They also had a more common onset of their infarction during heavy physical exertion (67% vs. 17%, P<0.001). A history of previous myocardial infarction, infarct location, global left ventricular function and regional wall motion were similar in both groups. After a mean follow-up period of 41±23 months, no patient died or had a second myocardial infarction in Group 1, and 4 patients had died in Group 2. The appearance of angina, less frequent in Group 1 than Group 2, tended to correlate with the extension of the coronary artery disease. We concluded that young patients with myocardial infarction have good prognosis irrespective of the coronary anatomy, although patients with normal coronary angiograms had less risk factors and less frequent new ischaemic events.     

Favorable effects of orally administered digoxin on left heart size and ventricular wall motion in patients with previous myocardial infarction.

The effects of maintenance oral digoxin therapy on segmental left ventricular wall motion (wall motion videotracking) and left heart size (radiographic left heart dimension) were evaluated in 14 patients with a prior myocardial infarction but without clinical signs or symptoms of congestive heart failure. The left heart dimension decreased in all six patients with cardiomegaly from an average of 55.0 +/- 1.6 (standard deviation) to 52.2 +/- 2.7 mm/m2 body surface area (P less than 0.01) during digoxin therapy. However, there was no significant change in the eight patients with normal heart size. In the resting state, the average extent of shortening in normal segments increased significantly from 3.1 +/- 0.8 to 4.2 +/- 1.2 mm during digoxin therapy. During submaximal handgrip exercise, the extent of shortening averaged 4.0 +/- 1.3 mm and increased further with digoxin therapy to 5.1 +/- 2.1 mm. The effects of digoxin therapy on the maximal velocity of shortening in normal segments at rest and during handgrip exercise were similar. In all 14 patients, there was a decrease in the number of segments with abnormal wall motion at rest or with handgrip exercise during digoxin therapy. With therapy, the number of abnormal sites decreased from 52 to 35 in the resting state and from 84 to 49 during handgrip exercise. Thus, in patients 6 or more months after transmural myocardial infarction, orally administered digoxin decreases cardiomegaly, increases the extent and maximal velocity of shortening in normal left ventricular segments and often reduces the extent of abnormal wall motion at rest or during isometric exercise.     

Assessment of mitral valve E point-septal separation as an index of left ventricular performance in patients with acute and previous myocardial infarction

A new echocardiographic index of left ventricular function, mitral valve E point-septal separation, was compared with the radionuclide ejection fraction determined using the first pass method in 60 patients (73 studies) with ischemic heart disease. Thirty-eight patients had acute myocardial infarction and 22 patients were studied an average of 24 months after acute infarction. In 30 normal subjects, E point-septal separation ranged from 0 to 5.4 mm (average 1.3 mm). In 57 studies (78 percent) E point-septal separation correctly identified patients with a normal or reduced ejection fraction (less than 0.52), but in 13 studies (18 percent) E point-septal separation was normal and ejection fraction depressed. In only three studies (4 percent) was there a normal ejection fraction and an abnormal E point-septal separation. Results did not differ between patients with acute infarction and those studied late after infarction. An E point-septal separation of more than 5.5 mm was highly specific (92 percent) for a reduced ejection fraction, but the sensitivity rate was only 65 percent. Abnormal wall motion as assessed with echocardiography or videotracking, or both, occurred equally among patients with normal and increased E point-septal separation, but this measure was less accurate in patients with more severe wall motion abnormalities. E point-septal separation was unrelated to heart rate; an abnormal value was equally distributed among patients with a normal and those with an enlarged left ventricular end-diastolic dimension on echocardiography. E point-septal separation was superior to other echocardiographic indexes of left ventricular function (percent of fractional shortening, mean rate of diameter shortening and ejection fraction). Thus, E point-septal separation is a simple noninvasive measure of left ventricular function. We conclude that an abnormal E point-septal separation is useful for identifying depressed left ventricular function in patients with acute myocardial infarction and chronic ischemic heart disease. However, 28 percent of our patients with a normal E point-septal separation had a depressed radionuclide ejection fraction. Therefore a normal value for E point-septal separation does not exclude the presence of abnormal left ventricular function in such patients.     

Posterior wall velocity: an unreliable index of total left ventricular performance in patients with coronary artery disease

Posterior wall velocity determined by use of echocardiography has been proposed as an index of total left ventricular performance in patients with ischemic heart disease. Accordingly, in 9 normal subjects and 39 patients with angiographically documented coronary artery disease, we compared mean endocardial posterior wall velocity determined by echocardiography with echocardiographic and biplane cineangiographic calculations of ejection fraction and the mean rate of circumferential fiber shortening (mean V_CF), and with externally recorded systolic time intervals. All studies were performed on the same day in each patient. Mean endocardial posterior wall velocity averaged 4.6 cm/sec (range 2.9 to 8.7) and correlated poorly with echocardiographic ejection fraction (r = 0.47), cineanglographic ejection fraction (r = 0.26), cineangiographic mean V_CF (r = 0.47), the ratio of preejection period to left ventricular ejection time (r = ?0.35) and the preejection period corrected for heart rate (r = ?0.30). Substitution of maximal for mean endocardial posterior wall velocity did not improve the separation of normal from depressed left ventricular performance. Epicardial posterior wall velocity, a measurement more easily obtainable than endocardial posterior wall velocity, also did not correlate well with systolic time intervals or with ejection fraction or mean v_cf derived from the echocardiogram and cineangiogram. Both endocardial and epicardial posterior wall velocity values were poorly reproducible on a day to day or a beat to beat basis. We conclude that neither endocardial nor epicardial posterior wall velocity, whether derived as a mean or a maximum, provides an accurate measure of total left ventricular performance in patients with coronary artery disease.     

Impaired parasympathetic responses in patients after myocardial infarction

To assess whether vagal and sympathetic responses are impaired 3 months after myocardial infarction, 27 patients, 15 age-matched control subjects and 13 young normal subjects underwent physiologic stress tests. In patients, facial immersion in water at 25 ° and 0 ° C provoked less slowing of heart rate than in age-matched control subjects. Young normal persons responded with the greatest reduction in heart rate. Response to facial immersion decreased linearly with age in normal subjects (Y = −0.97X + 86). Isometric handgrip or cold pressor test elicited brisk increases in blood pressure in almost all patients, but the vagal response to facial immersion correlated poorly with such pressor responses. Thus, in the patients studied 3 months after myocardial infarction, the parasympathetic response to facial immersion was significantly impaired whereas sympathetic pressor responses remained intact.     

Favorable effects of oral maintenance digoxin therapy on left ventricular performance in normal subjects: Echocardiographic study

Left ventricular performance was assessed with echocardiography in 10 normal subjects before and during maintenance therapy with digoxin (0.5 mg/day orally) in the basal state and after acute pressure loading with intravenously administered phenylephrine. During digoxin therapy, despite a decrease in mean heart rate of 5 beats/min in the basal state, mean left ventricular ejection fraction increased from 74 ± 2 to 79 ± 1 percent (standard error, P < 0.03); percent shortening of a left ventricular minor dimension increased from 37 ± 2 to 41 ± 1 percent (P < 0.04) and the mean rate of left ventricular dimension shortening increased from 5.66 ± 0.22 to 6.31 ± 0.23 cm/sec (P = 0.05). During acute pressure loading with phenylephrine there was no change in mean heart rate after digoxin and mean ejection fraction increased from 69 ± 3 to 75 ± 2 percent; mean percent shortening increased from 33 ± 2 to 38 ± 2 percent; mean rate of shortening increased from 5.46 ± 0.32 to 6.48 ± 0.33 cm/sec and mean normalized rate of shortening increased from 1.11 ± 0.06 to 1.29 ± 0.05 sec⁻¹ (all P < 0.01). In a few subjects the response to digoxin did not coincide with the mean data for the whole group. This variability was largely due to difficulties in exactly matching heart rate between the control and digoxin studies. These data (1) support the concept that long-term oral digoxin therapy exerts a positive inotropic effect on the normal left ventricle, and (2) demonstrate the usefulness of echocardiography in noninvasive assessment of the effects of drugs on left ventricular performance.     

Cardiokymography: Quantitative analysis of regional ischemic left ventricular dysfunction

Regional anterior left ventricular function was analyzed with cardiokymography in 24 patients undergoing diagnostic cardiac catheterization for suspected coronary artery disease. The noninvaslve kymographic tracing was recorded simultaneously with left ventricular pressure and normalized for differences in amplification. In 10 patients with normal anterior wall motion on ventriculography, the cardiokymogram revealed uniform inward motion during ejection, comprising 88 ± 4 percent (mean ± standard error of the mean) of total amplitude. Little change in amplitude was observed during isovolumic relaxation (−3 ± 7 percent). The remaining 14 patients all had significant coronary artery disease affecting the anterior wall of the left ventricle. In seven patients, with anterior dyssynchrony or hypokinesia, or both, the cardiokymogram revealed a significant decrease in systolic inward motion to 57 ± 9 percent of total amplitude (P < 0.002) and a significant increase in isovolumic relaxation amplitude to 35 ± 18 percent (P < 0.02). In the other seven patients, with anterior aklnesla or dyskinesia, or both, the cardiokymogram exhibited outward rather than Inward motion during ejection (−40 ± 11 percent).

These observations in man are similar to those made with directly Implanted length gauges or ultrasonic crystals in animals subjected to acute myocardial ischemia. The data suggest that cardiokymography is capable of providing a clinical nonlnvaslve analog tracing that corresponds to normal and ischemic left ventricular wall motion. The technique therefore appears applicable to the noninvasive detection and serial evaluation of regional Ischemic contraction abnormalities in man.     

Improved right ventricular systolic time intravals after digitalis in patients with cor pulmonale and chronic obstructive pulmonary disease

Although digitalis has been used to treat patients with cor pulmonale secondary to chronic obstructive pulmonary disease, its effect on right ventricular performance has not been conclusively determined. This study assessed the effects of acute digitalization on measurement of right ventricular systolic time intervals in patients with chronic obstructive pulmonary disease and cor pulmonale. The intervals were recorded before and 40 minutes after administration of ouabain, 1 mg intravenously, in nine men (mean age 58 ± 5 [standard deviation] years) with chronic obstructive pulmonary disease (mean maximal mid expiratory flow rate 0.29 ± 0.08 1 liters/sec) and electrocardiographic evidence of right ventricular hypertrophy.

Ouabain produced significant reductions in right ventricular systolic time intervals, including the right ventricular preelection period (from 117 ± 23 to 102 ± 16 msec; P < 0.01), right ventricular ejection time index (from 397 ± 33 to 375 ± 24 msec; P < 0.01) and mean Q-P₂ index (from 509 ± 23 to 474 ± 8 msec; P < 0.001). In eight patients with simultaneously measured left ventricular systolic time intervals, similar changes were observed, including shortening of the left ventricular preejection period index (from 135 ± 9 to 117 ± 11 msec; P < 0.01), ejection time index (from 395 ± 18 to 379 ± 20 msec; P < 0.01), and the mean Q-A₂ interval (from 530 ± 16 to 495 ± 16 msec; P < 0.001). There were no significant changes in aortic or pulmonary arterial pressures. The results demonstrate that acute administration of digitalis produces significant improvement in right ventricular performance in patients with chronic obstructive pulmonary disease and cor pulmonale. The simultaneous shortening of right and left ventricular systolic time intervals is of comparable magnitude.     

Effect of pulsatile and nonpulsatile flow during cardiopulmonary bypass on left ventricular ejection fraction early after aortocoronary bypass surgery

Although aortocoronary bypass graft has successfully relieved angina in most patients, concern has been expressed about possible deterioration or failure of improvement of left ventricular performance. With use of intraaortic balloon pumping to produce pulsatile flow during cardiopulmonary bypass, left ventricular ejection fraction and end-diastolic volume index were compared in a consecutive series of 40 men undergoing elective aortocoronary bypass, 20 of whom had pulsatile flow and 20 who had mean flow during cardiopulmonary bypass. Left ventricular ejection fraction and end-diastolic volume index were measured before and 1 to 12 days after operation using a collimated scintillation probe and indium^113m. In the group receiving nonpulsatile flow the ejection fraction decreased from 52.2 ± 2.9 percent (mean ± standard error of the mean) to 38.7 ± 3.2 percent on the first postoperative day and 43.0 ± 3.4 percent on the 10th day (P < 0.001). In the group receiving pulsatile flow, the ejection fraction increased from 51.4 ± 3.0 percent to 61.6 ± 3.4 percent on day 1 and 65.8 ± 2.9 percent on day 10 (P < 0.001). Three of 20 (15 percent) in the group with nonpulsatile flow had an increase of ejection fraction compared with 17 of 20 (85 percent) in the group given pulsatile flow. Left ventricular end-diastolic volume index was not significantly altered in either group. Two men (10 percent) in each group had post-operative myocardial infarction. The ejection fraction increased despite infarction in both patients given pulsatile flow but decreased in both patients with infarction given mean flow. In a series of 235 patients intraoperative infarction occurred in 8 of 109 patients given pulsatile flow (incidence 7.3 percent) but in 14 of 126 patients given mean flow (incidence 11.1 percent) (P < 0.05). These results suggest that pulsatile flow during cardiopulmonary bypass (1) improves left ventricular ejection fraction in the early postoperative period in patients undergoing aortocoronary bypass and (2) may enhance myocardial preservation in these patients.     

Left ventricular function at rest and during exercise after aortic valve replacement in patients with aortic regurgitation

To determine the effect of aortic valve replacement on reversing abnormalities of left ventricular function in patients with aortic regurgitation, radionuclide cineangiography was used to study 16 symptomatic patients with aortic regurgitation before and 6 months after aortic valve replacement. Before operation, left ventricular ejection fraction was 46 ± 3 percent at rest (normal mean ± standard error of the mean 57 ± 1 percent; P < 0.001), and decreased to 37 ± 4 percent during exercise (normal 71 ± 2 percent; P < 0.001). After operation, ejection fraction rose to 58 ± 4 percent at rest, indistinguishable from the normal value, and during exercise was 53 ± 4 percent, increased (P < 0.001) from before operation but significantly (P < 0.001) subnormal. Thus, aortic valve replacement can improve but usually does not normalize left ventricular function during exercise in symptomatic patients with aortic regurgitation.     

Spectrum of coronary arterial spasm. Clinical, angiographic and myocardial metabolic experience in 29 cases

A relationship of coronary arterial spasm to variant angina pectoris, subendocardial ischemia, major ventricular arrhythmias and myocardial infarction has been demonstrated. In 29 patients, spasm was angiographically observed in normal-appearing coronary arteries (7 patients) as well as superimposed on various degrees of coronary atherosclerotic obstruction (22 patients). All patients experienced an atypical anginal syndrome; 16 patients also experienced typical exertional angina. Coronary spasm appeared to be a major contributory factor in eight occurrences of myocardial infarction and in 11 incidents of ventricular tachycardia, ventricular fibrillation and heart block.

Coronary spasm in the 29 cases was distributed in the following fashion: left main trunk, 6 cases; right main trunk, 12 cases; proximal left anterior descending artery, 13 cases; proximal circumflex artery, 1 case; distal left anterior descending artery, 1 case; and distal circumflex artery, 2 cases. In 5 cases coronary spasm was noted at multiple sites.

In contrast to findings in patients manifesting only typical exertional angina, the hemodynamic findings during spasm were those of a hypodynamic state. Left ventricular systolic pressure decreased from 138.9 ± 6.0 (mean ± standard error of the mean) to 113.2 ± 6.2 mm Hg; left ventricular end-diastolic pressure did not change significantly. Myocardial lactate extraction during spasm was invariably markedly reduced: −53.19 percent ± 15.44 (P < 0.001). However, the effect of coronary sinus pacing on myocardial lactate extraction was not significantly abnormal: +15.74 percent ± 6.66.

The respective roles of medical and surgical intervention are uncertain. Only 3 patients had a completely satisfactory pharmacologic response to nitrates alone or in combination with propranolol, and the condition of 5 others was partially improved; the remaining 21 patients were judged intractable to medical management. Coronary bypass surgery was performed as the ultimate recourse in 18 patients. However, short-term results reveal that only nine (50 percent) showed improvement, four (22 percent) had myocardial infarction during or after surgery and four (22 percent) died.

These studies confirm that coronary arterial spasm is a definite pathogenetic factor in a variety of acute myocardial ischemic syndromes. The incidence and full clinical significance of this functional disorder remain to be determined.     

Medical and surgical management of myocardial infarction

The in-hospital and long-term mortality (18 to 56 months) of two groups of patients treated concurrently for acute transmural myocardial infarction are retrospectively compared. Group I (no. = 200) was given medical therapy, whereas Group II (no. = 187) underwent early coronary arterial bypass grafting. The groups were comparable in average age, incidence of previous myocardial infarctions, initial electrocardiographic findings (S-T segment elevation), area of electrocardiographic involvement, initial cardiac enzyme activity, coronary anatomy (when known) and Killip classes I to III on admission to the study. Significantly more patients in Group II were in Killip clinical class IV.

In-hospital mortality was lower in Group II than in Group I without (5.8 versus 11.5 percent) and with (1.2 versus 9.3 percent [P < 0.003]) exclusion of class IV patients from both groups. Long-term mortality during the observation period (18 to 56 months) was also lower in Group II without and with exclusion of class IV patients (11.7 versus 20.5 percent [P < 0.03] and 7.1 versus 18.1 percent [P < 0.005], respectively).

Group II was arbitrarily classified into two subgroups. Patients in subgroup IIA (no. 110) had abnormally elevated total creatine kinase (CK) activity (more than 90 IU) preoperatively and were placed on cardiopulmonary bypass 9.3 ± 2.6 hours (mean ± standard error of the mean) from the onset of symptoms. The in-hospital and long-term mortality rates were not significantly different from those in Group I (8.1 versus 11.5 percent and 17.2 versus 20.5 percent, respectively). Patients in subgroup IIB (no. = 77) had normal serum CK activity preoperatively and were placed on cardiopulmonary bypass 5.3 ± 1.4 hours from the onset of symptoms. The in-hospital and long-term mortality rates were significantly lower than those in Group I (2.6 versus 11.5 percent [P < 0.01] and 3.9 versus 20.5 percent [P < 0.001], respectively). In the 100 patients in Group II placed on cardiopulmonary bypass within 6 hours of symptoms regardless of CK activity, in-hospital and long-term mortality rates were significantly lower than in patients receiving medical therapy (2.0 versus 11.5 percent [P < 0.01] and 6.0 versus 20.5 percent [P < 0.001), respectively. Of the 100 patients, 46 were from subgroup IIA and 54 from subgroup IIB. The inhospital mortality rate was 2.1 percent (1 of 46) and 1.8 percent (1 of 54), respectively.

These preliminary data suggest that if the result of surgical reperfusion as treatment for acute evolving myocardial infarction is to be significantly different from that of medical management, reperfusion must be performed early in the course of infarction. A controlled randomized trial is suggested     

Coronary dilatory capacity in idiopathic dilated cardiomyopathy: Analysis of 16 patients

Hemodynamic function and overall coronary blood flow (argon technique) were measured in 16 patients with idiopathic dilated cardiomyopathy (IDC) and in 12 patients without detectable heart disease (control subjects) referred for precordial pain. In patients with IDC, coronary blood flow was normal at rest (78 ± 17 ml/100 g·min versus 78 ± 9 in control subjects). During maximal inducible coronary vasodilation (dipyridamole, 0.5 mg/kg), coronary blood flow was significantly reduced (142 ± 38 ml/100 g · min versus 301 ± 64 in control subjects; p < 0.001). Consequently, obtainable minimal coronary resistance was increased in IDC (0.54 ± 0.20 mm Hg/ml/100 g · min versus 0.23 ± 0.04 in control subjects; p < 0.001). In patients with IDC, left ventricular (LV) end-diastolic pressure was significantly increased (19 ± 11 mm Hg versus 6 ± 3 in control subjects; p < 0.005), and the LV ejection fraction was diminished (36 ± 11% versus 72 ± 3% in control subjects; p < 0.001). In patients with IDC, LV end-diastolic pressure correlated significantly with the obtained minimal coronary resistance after application of dipyridamole (r = 0.85; p < 0.001). LV catheter biopsy specimens revealed no alterations in myocardial microvasculature. Thus, coronary dilatory capacity is impaired in patients with IDC, due partially to an increase in extravascular component of coronary resistance.     

Exercise training soon after myocardial infarction

To assess the cardiovascular effects of exercise training soon after clinically uncomplicated myocardial infarction, 70 men (mean age 54 years) underwent gymnasium training (no. = 28), home training (no. = 12) or no training (no. = 30) 3 to 11 weeks after the acute event. During this 8 week interval functional capacity increased significantly (P < 0.001) in all three groups: gymnasium training, 66 percent; home training, 41 percent; and no training, 34 percent. Peak functional capacity at 11 weeks was 11.0 ± 1.6, 10.3 ± 1.4 and 9.4 ± 1.8 (mean ± standard deviation) multiples of resting energy expenditure (METs) in the three groups—values approximating those of sedentary men of similar age without coronary heart disease. Functional capacity increased more in the gymnasium training group than in the no training group, but this difference was statistically significant only in patients without exercise-induced ischemie S-T segment depression or angina pectoris (P < 0.01). Another “training effect”—diminished heart rate response to submaximal work—was also observed in all three groups. It is concluded that (1) symptom-limited treadmill exercise testing performed soon after clinically uncomplicated myocardial infarction is feasible and safe and provides useful guidelines for physical reconditioning. (2) Patients who demonstrate nonischemic responses to treadmill exercise testing soon after infarction may safely undergo unsupervised exercise training at home. (3) Formal exercise training may not be required to restore functional capacity to nearly normal values soon after clinically uncomplicated myocardial infarction.     

Dynamic change in collateral flow associated with myocardial ischemia in humans

Background: This study sought to investigate how collateral flow changes during myocardial ischemia in patients. Methods: Myocardial contrast echocardiography (MCE) and rapid atrial pacing were performed in 20 patients with angiographically evidenced coronary collaterals from the right coronary artery (RCA) to the occluded left anterior descending coronary artery. Sonicated contrast medium was injected into the RCA before and immediately after atrial pacing to determine the peak background-subtracted contrast intensity (PI) in the collateral territory (PIA) and its ratio to PI in the control territory (PI ratio) as parameters of collateral blood flow. Lactate production in the coronary circulation during pacing was determined to assess myocardial ischemia in the collateral territory. Results: PIA showed a significant correlation with regional wall motion either before (r(squared)=−0.64, P<0.01) or after pacing (r(squared)=−0.65, P<0.01). Similarly, PI ratio was significantly correlated with regional wall motion either before (r(squared)=−0.54, P<0.05) or after pacing (r(squared)=−0.64, P<0.01). Rapid atrial pacing decreased both PIA and PI ratio significantly greater in patients with lactate production than in those without (PIA: −67±53 vs. −15±34%, P<0.05; PI ratio: −68±49 vs. −8.2±32%, P<0.05, respectively), while neither PIA nor PI ratio differ between the two groups of patients before pacing (PIA: 13.8±19. vs. 16.2±13.3U, P=0.75; PI ratio: 0.70±0.71 vs. 0.87±0.65, P=0.58, respectively). Conclusions: We concluded that (1) collateral flow determined by MCE was closely associated with regional cardiac function, and (2) not the amount of collateral flow at rest, but pacing-induced change of collateral flow seemed to be a determinant of regional ischemia in patients with coronary collaterals.     

Magnitude of myocardial dysfunction is greater in painful than in painless myocardial ischemia: An exercise echocardiographic study

Objectives. This study sought to assess the presence and extent of inducible myocardial dysfunction during painful and painless (silent) myocardial ischemia in a homogeneous patient cohort with coronary artery disease and no previous myocardial infarction.

Background. The functional significance of painless versus painful demand-driven ischemia remains controversial, with conflicting results in published reports regarding the amount of myocardium in jeopardy.

Methods. Exercise echocardiography was performed in 89 patients (mean [±SD] age 59.3 ± 8.2 years) with significant coronary artery disease and positive exercise stress test results. Patients were taking no antianginal medications and were classified into painless and painful cohorts after the outcome of a symptom-limited treadmill exercise test. No patients had previous coronary artery bypass surgery. Images were acquired in digital format before and immediately after treadmill exercise testing.

Results. Fifty-eight patients had painful and 31 painless myocardial ischemia. Clinical and demographic characteristics as well as coronary artery anatomy were similar in both groups. Patients with painless ischemia achieved better exercise performance with greater exercise duration (p < 0.001) and higher maximal rate-blood pressure product (p < 0.001) than those with painful ischemia. New wall motion abnormalities were seen in 54 patients (93%) with painful versus 17 (55%) with painless ischemia (p < 0.001). Total ischemic score was greater in patients with painful than in those with painless ischemia (15.9 ± 3.7 vs. 12 ± 1.4, p < 0.001, respectively), with a greater number of ischemic myocardial segments in painful than in painless ischemia (101 [16%] vs. 21 [6%], p < 0.001, respectively).

Conclusions. Patients with painless ischemia frequently have regional myocardial dysfunction on exertion detected by echocardiography, but painful episodes are accompanied by a greater magnitude of myocardial dysfunction.