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To evaluate the possible irreversibility of isometric exercise-induced left ventricular dysfunction in aortic regurgitation, we performed handgrip exercise tests during cardiac catheterization on 17 patients with chronic aortic regurgitation (AR-group), both preoperatively and one year after successful aortic valve replacement. Nine normal subjects served as a control group. Preoperatively, the ejection fraction decreased from 59 ± 7% to 53 ± 8% (P<0.001) in the AR-group while it remained unchanged in the control group during exercise. A positive correlation existed between the changes in the ejection fraction during pre- and postoperative exercise tests (r = 0.85, P < 0.001), which revealed that in patients with severely depressed ejection fraction during the preoperative exercise test, the ventricular response to exercise was not totally corrected after surgery. The regression of left ventricular mass was also smaller in the patients with most depressed ventricular response to exercise preoperatively. As the isometric exercise-induced left ventricular dysfunction appears to be partly irreversible, we conclude that the valve replacement should perhaps be performed before stress-induced ventricular dysfunction has occurred. Non-invasive monitoring of ventricular response to exercise might be helpful in optimizing the timing of valve replacement in aortic regurgitation. [ABSTRACT FROM PUBLISHER]

OBJECTIVES--To study the risk factors for cardiac mortality after coronary artery bypass graft surgery. DESIGN AND SETTING--Follow up study of patients who had undergone coronary artery bypass graft surgery at the University Hospital of Oulu, Finland. PATIENTS AND INTERVENTIONS--339 consecutive patients who underwent cardiac catheterisation three months after bypass surgery. MAIN OUTCOME MEASURES--Incidence of cardiac deaths during the follow up period of five years and predictive value of clinical and angiographic variables for subsequent cardiac mortality. RESULTS--The incidence of cardiac deaths was 5.1%, and 81% of these were sudden deaths. The postoperative ejection fraction was significantly lower in the patients with subsequent cardiac death than in the survivors (p less than 0.001), and their left ventricular end systolic and end diastolic volumes were higher (p less than 0.001 and p less than 0.05 respectively). The incidence of cardiac deaths was 43% in the patients with a postoperative ejection fraction of less than 40%. The myocardial jeopardy index after surgery and the rate of graft patency were not significantly different in the survivors and patients who died. The only clinical factors that were different between the groups were postoperative use of diuretics (p less than 0.001) or digitalis (p = 0.02). After adjustment for other prognostic variables by the proportional hazards method, a low postoperative ejection fraction remained significant as a predictor of the relative risk of cardiac mortality five years after operation (p less than 0.01). CONCLUSIONS--Patients with angiographic evidence of impaired left ventricular function after bypass surgery are still at relatively high risk of dying suddenly, but myocardial ischaemia due to incomplete revascularisation is not strongly associated with an increased risk of cardiac mortality. Conventional clinical methods do not seem to be helpful for identifying patients with an increased risk of cardiac death after bypass surgery. [ABSTRACT FROM PUBLISHER]

Thallium tomographic imaging and exercise electrocardiography were performed on 136 diabetic patients without symptoms of heart disease. Thirty three patients had post-exercise thallium defects and 19 had ST 1 mm greater than or equal to segment depression during exercise electrocardiography. Both tests were positive in 13 patients. Coronary angiography was subsequently performed on 33 patients with either scintigraphic and/or electrocardiographic evidence of myocardial ischaemia. Angiographically significant coronary artery disease (greater than or equal to 50% narrowing of the coronary artery lumen) was detected in 13 patients. Six patients had minimal coronary artery stenosis (less than 50%), and 14 had normal coronary arteries. Six patients refused cardiac catheterisation. In 14 out of 27 patients with post-exercise thallium defects coronary angiography did not show any coronary artery stenoses (positive predictive accuracy 48%). Exercise electrocardiography showed only one false positive result (positive predictive accuracy 94%) but failed to detect coronary artery disease in three patients with a positive scintigraphic result. The accuracy of a positive exercise electrocardiographic test seems to be better than that of a positive thallium tomographic scan for detecting asymptomatic coronary artery disease in diabetic patients. The high number of false positive thallium defects may be the result of technical features inherent in thallium tomography and/or the possible disease of the small intramyocardial arteries in diabetic patients. [ABSTRACT FROM PUBLISHER]

Heart rate variation in deep breathing, a sensitive non-invasive measure of cardiac parasympathetic activity, was measured in 63 patients with coronary artery disease, in 22 patients with atypical chest pain, and in 20 healthy symptom free volunteers. There was significantly less heart rate variation in deep breathing in the patients with coronary artery disease than in the healthy subjects. Twenty patients (32%) with coronary artery disease had lower than normal variation in heart rate. The patients with chest pain showed an intermediate heart rate response to deep breathing. Sinus arrhythmia in the patients with coronary artery disease was not related to the functional class, medication, number or location of narrowed vessels, or to the left ventricular ejection fraction, and end diastolic pressure. These results suggest that impairment of the parasympathetic nervous function is common in coronary artery disease. [ABSTRACT FROM PUBLISHER]

The relative significance of the direct and indirect effects of autonomic tone on diurnal fluctuations in human ventricular and atrial refractoriness are not well known. In this study, the circadian rhythms of ventricular and atrial effective refractory periods (ERPs) were measured by noninvasive programmed stimulation in ten patients (mean age 62 +/- 10 years) who had a permanent dual chamber pacemaker for complete atrioventricular (AV) block. The ERP was measured at 4-hour intervals during spontaneous sinus rhythm with ventricular pacing (day 1) and during constant-rate dual chamber pacing (day 2). Cosinor analysis showed the ventricular ERP to have a significant diurnal rhythm in sinus rhythm (amplitude, 12 msec; 95% confidence intervals 1-24 msec) but not during constant-rate pacing (amplitude, 4 msec; 95% confidence intervals -3-12 msec). The atrial ERP had a significant rhythm at times of both spontaneous sinus rate (amplitude, 19 msec; confidence intervals 13-24 msec) and constant heart rate (amplitude, 11 msec; confidence intervals 1-21 msec) with acrophase during the sleeping hours. The increase in heart rate during dual chamber pacing resulted in a more marked decrease in the average 24-hour ERP in the ventricle than in the atrium (46 +/- 9 msec vs 12 +/- 6 msec, P < 0.01). Thus, refractoriness is more rate dependent in the ventricle than in the atrium, and autonomic influences on ventricular refractoriness are mainly indirect, via fluctuations in the sinus rate, but atrial refractoriness is also affected by direct neural influences and/or other rate independent factors.

Autonomic mechanisms may have an important role in the clinical presentation of acute coronary occlusion. This research was designed to evaluate the effect of preocclusion stenosis severity on the immediate autonomic heart rate (HR) responses to a subsequent acute occlusion of the coronary artery. HR and its variability in the time and frequency domains were analyzed in patients with mild to moderate (< or = 85%) (group 1, n = 19) and severe (> 85%) (group 2, n = 18) left anterior descending coronary artery stenosis immediately before and during balloon occlusion (mean 108 seconds). The ranges of nonspecific responses were determined by analyzing HR reactions in a control group (n = 13) with no ischemia during balloon inflation of a totally occluded coronary artery. An abnormal increase in HR variability and/or bradycardia as a sign of vagal activation occurred in 6 patients (32%) in group 1 and in 3 patients (17%) in group 2. A significant decrease in HR variability or tachycardia, or both, was observed in 5 patients (26%) in group 1, but in none of the patients in group 2. Compared with the control group, the balloon occlusion of mild to moderate stenosis caused abnormal HR reactions more often than did occlusion of tight stenosis (58% vs 17%, p < 0.05). Balloon occlusions in group 1 caused chest pain (p < 0.01), ST-segment changes (p < 0.001), and narrowing of pulse pressure (p < 0.05) more often than did occlusions of severe stenoses.(ABSTRACT TRUNCATED AT 250 WORDS)

Reduced heart rate (HR) variability is associated with increased risk of cardiac arrest in patients with coronary artery disease. In this study, the power spectral components of HR variability and their circadian pattern in 22 survivors of out-of-hospital cardiac arrest not associated with acute myocardial infarction were compared with those of 22 control patients matched with respect to age, sex, previous myocardial infarction, ejection fraction and number of diseased coronary arteries. Survivors of cardiac arrest had significantly lower 24-hour average standard deviation of RR intervals than control patients (29 +/- 10 vs 51 +/- 15 ms, p less than 0.001), and the 24-hour mean high frequency spectral area was also lower in survivors of cardiac arrest than in control patients (13 +/- 7 ms2 x 10 vs 28 +/- 14 ms2 x 10, p less than 0.01). In a single cosinor analysis, a significant circadian rhythm of HR variability was observed in both groups with the acrophase of standard deviation of RR intervals and high-frequency spectral area occurring between 3 and 6 A.M. which was followed by an abrupt decrease in HR variability after arousal. The amplitude of the circadian rhythm of HR variability did not differ between the groups. Thus, HR variability is reduced in survivors of cardiac arrest but its circadian rhythm is maintained so that a very low HR variability is observed in the morning after awakening, corresponding to the time period at which the incidence of sudden cardiac death is highest.

The predictive value of a postoperative exercise test in terms of cardiac events after coronary artery bypass grafting (CABG) was prospectively studied in 231 consecutive patients. During a 5-year follow-up there were 28 cardiac events (12%), of which 15 were cardiac deaths (13 sudden), and 13 were nonfatal myocardial infarctions. There was no difference in the rate of graft patency between groups with and without cardiac events, but ejection fraction was lower in patients with than without events (51 +/- 16% vs 58 +/- 10%; p less than 0.05). Duration of the exercise test was shorter, and maximal work load was lower in patients with cardiac events (p less than 0.05 for both). The prevalence of greater than or equal to 1 mm ST-segment depression was 22% (symptomatic in 25%, and silent in 75%) and did not differ between groups with and without cardiac events. After adjustment for prognostic variables using the proportional hazards method, diuretic treatment (p = 0.007) and a low postoperative ejection fraction (p = 0.04) remained significant for predicting the risk of cardiac events within 5 years of CABG, but exercise duration and work load did not have any significant predictive value. Thus, the predictive value of a postoperative exercise test is limited, and signs of impaired left ventricular function are of greater significance for the 5-year prognosis after CABG than are those of myocardial ischemia.

Sudden cardiac death and ischaemic cardiac events occur in a circadian pattern. Because ventricular tachycardia is thought to play an important role in sudden cardiac death, the episodes of spontaneous ventricular tachycardias (greater than 3 consecutive beats) (n = 1314) were analysed from 24-hour long term electrocardiographic recordings in 34 patients with coronary arterial disease to determine whether circadian rhythm exists in spontaneous ventricular tachycardia. Twelve patients had suffered cardiac arrest, four patients had a history of syncope, and palpitation was the indication for electrocardiographic recordings in eighteen patients. Analysis using chronobiologic single cosinor method showed a significant circadian variation in the occurrence of ventricular tachycardia episodes with the peak occurring at 6 a.m. Similar circadian rhythm was also observed in the occurrence of the longest episode of ventricular tachycardia. Ischaemic ST-segment depression preceded the longest ventricular tachycardia episode only in one patient. Thus, a circadian rhythm occurs also in spontaneous episodes of ventricular tachycardia, a finding which is similar to that in sudden cardiac death.

To elucidate the potential association of diabetic autonomic neuropathy with increased prevalence of silent coronary artery disease (CAD), 138 asymptomatic diabetic subjects were screened using exercise ECG. 24-h ambulatory ECG and dynamic thallium scintigraphy. Fourteen patients with exercise-induced myocardial ischaemia and angiographically confirmed CAD (greater than or equal to 50% coronary artery narrowing) were found using this protocol. Their autonomic nervous function was assessed using standard cardiovascular tests and compared with that of 23 consecutive diabetic patients catheterised because of symptomatic CAD (mean New York Heart Association class 3.0). The diabetic patients with symptomatic CAD had more severe coronary atherosclerosis than the diabetic patients with asymptomatic CAD assessed by jeopardy score (P less than 0.01). The groups did not, however, differ with respect to autonomic function tests. Five patients (22%) with symptomatic CAD and 3 patients (21%) with asymptomatic CAD had definite autonomic dysfunction, i.e. two or more abnormal tests. Thus, our results suggest that the frequency of autonomic neuropathy is not increased in diabetic patients with asymptomatic CAD. The contribution of diabetic autonomic neuropathy to the absence of cardiac pain needs further clinical and pathological studies.

Diminished variation in heart rate as a sign of impaired vagal control is common in coronary arterial disease. To evaluate the effect of short-term myocardial ischaemia induced by coronary arterial occlusion during therapeutic percutaneous transluminal coronary angioplasty we measured the variation in heart rate during controlled deep breathing in 50 patients before and during arterial occlusion. Variation in heart rate diminished from 11.1 +/- 4.5 to 9.5 +/- 5.1 beats/min (P less than 0.01) during occlusion. No change occurred in heart rate, blood pressure or levels of noradrenaline and adrenaline. The attenuation of variation in the heart rate was not significantly associated with the site or duration of arterial occlusion nor concomitant chest pain. Thus, brief coronary arterial occlusion seems to be associated with impairment of the vagal control of heart rate in patients with coronary arterial disease.

Exercise-induced ventricular arrhythmias occur often after coronary artery bypass grafting (CABG), but their prognostic significance is unknown. Two hundred patients examined by exercise electrocardiography and cardiac catheterization (including left ventriculography, bypass graft and native coronary artery angiography) before and 3 months after CABG were prospectively followed up. Exercise-induced ventricular arrhythmias occurred more often after (49 of 200 patients, 24.5%) than before (32 of 200 patients, 16.0%) CABG (p less than 0.05). There were no differences between the patients with and without ventricular arrhythmias in the prevalence of graft patency (79 vs 80%) or the postoperative ejection fraction (57 +/- 9 vs 57 +/- 12%). Ten cardiac deaths occurred during the mean follow-up time of 61 +/- 19 months, 8 of which were witnessed sudden cardiac deaths. All cardiac deaths occurred in patients who did not have exercise-induced ventricular arrhythmias after CABG. The postoperative ejection fraction was lower in the cardiac death patients (42 +/- 16%) than in the survivors (58 +/- 10%) (p less than 0.01). No other clinical or angiographic variable predicted the occurrence of cardiac death. Thus, the prevalence of exercise-induced ventricular arrhythmias increases after CABG, but the occurrence of ventricular arrhythmias does not indicate an increased risk of cardiac death.

To assess the prevalence and long-term prognostic significance of complex ventricular arrhythmias after coronary arterial bypass graft surgery, 126 patients were studied by 24-hour ambulatory electrocardiographic recordings and cardiac catheterizations (including left ventricular, coronary arterial and bypass graft angiograms) before and 3 months after surgery, and then prospectively followed-up for a mean of 50 months. Complex ventricular arrhythmias (ventricular premature complexes greater than 30/hour, multiform and/or repetitive complexes) occurred more commonly after than before surgery (in 49/126 vs. 30/126 patients, P less than 0.05). In 18 patients (14%) who had significant worsening of ventricular arrhythmias, the ejection fraction decreased significantly (from 56 +/- 13% to 50 +/- 15%, P less than 0.05) after operation. During the period of follow-up, there were 4 witnessed sudden cardiac deaths. Complex ventricular arrhythmias tended to be more prevalent in patients who died suddenly (in 100%) compared to survivors (in 37%), but their presence did not predict the subsequent sudden death when ejection fraction was included in the stepwise regression model. None of the patients with an ejection fraction over 40% suffered sudden death despite the prevalence of complex arrhythmias in 32% of these patients. Thus, complex ventricular arrhythmias tend to occur more frequently after than before bypass surgery and their occurrence appears to be related to impairment of left ventricular function. Patients with well preserved ventricular function are at low risk of dying suddenly despite presence of complex ventricular arrhythmias after surgery.

Echocardiography was performed on 71 young (mean age 26 years) insulin-dependent diabetic women without clinical evidence of heart disease and on 36 healthy women of the same age. 39 diabetic women had microvascular complications and 9 of them also had abnormalities in autonomic function tests. The diabetic women had smaller left ventricular (LV) end-diastolic diameters (44 vs. 47 mm, p less than 0.001) than the controls, although the left atrial sizes did not differ between the groups. They also had higher heart rates (80 vs. 70 bpm, p less than 0.001) and shortening fractions (35 vs. 33%, p less than 0.01), smaller stroke volumes (66 vs. 76 ml, p less than 0.01) and thicker interventricular septae (9 vs. 8 mm, p less than 0.01) than the controls. The diminution of LV size was most prominent in patients with severe microvascular complications. These data suggest that the myocardial contractility of young insulin-dependent diabetic women is not depressed, but rather exaggerated. The observed diminution of LV size in combination with normal left atrial diameter may reflect increased LV wall stiffness, a possible pre-clinical manifestation of the specific heart disease of diabetes.

In order to evaluate the left ventricular response to isometric exercise in different types of aortic valve disease, isometric exercise tests were performed during cardiac catheterization in 14 patients with pure aortic stenosis, 20 with combined aortic stenosis and regurgitation, and 18 with pure aortic regurgitation. Patients with angina pectoris in whom coronary angiography had not been performed were excluded. Thirty-seven patients were recatheterized 12 months after aortic valve replacement, and the ventricular response to exercise was re-evaluated. Preoperatively, the ejection fraction did not change significantly during exercise in patients with aortic stenosis, tended to decrease in patients with combined valve lesion, and decreased significantly in patients with aortic regurgitation (p less than 0.001). In the three patients whose ejection fraction during preoperative exercise decreased to below 0.40, it remained below 0.50 after successful aortic valve replacement. It appears possible to reveal left ventricular dysfunction in many patients with aortic regurgitation and in some with combined aortic valve disease by means of isometric exercise. The severely depressed ventricular dysfunction during exercise does not appear to correct totally after surgery.

To investigate the incidence and clinical significance of postoperative pericardial effusion (PE), the presence of PE was evaluated by echocardiography, 1 and 2 weeks postoperatively, in 50 patients after insertion of a valve prosthesis and in 100 patients after coronary bypass surgery (50 patients receiving a combination of aspirin and dipyridamole and 50 receiving warfarin). PE was found during either procedure in 77% of patients and was marked in 29%. Symptoms of postpericardiotomy syndrome (p less than 0.05), pericardial friction rub (p less than 0.01), atrial arrhythmias (p less than 0.05), cardiac enlargement (p less than 0.01), and pleural effusion (p less than 0.05) were detected more frequently in patients with PE than in those without PE. PE was not related to the type of antithrombotic therapy, the rate of coronary bypass graft occlusion, or the type of cardiac surgery. However, the use of the left internal mammary artery as a coronary bypass graft was associated with a slightly higher incidence of PE (p less than 0.05). One patient (0.7%) required surgical drainage of PE. It was concluded that PE is a common and benign finding after cardiac surgery and usually disappears without specific therapy.

We measured the variation in heart rate during deep breathing, a sensitive non-invasive measure of cardiac parasympathetic activity, in 95 patients 3 weeks after myocardial infarction and in 40 asymptomatic healthy controls. The variation in rate was significantly lower (11.6 +/- 6.1 vs 17.6 +/- 7.3 beats/min, P less than 0.001) in patients with myocardial infarction than in controls. Forty-nine patients (52%) and 5 controls (13%) were considered to have diminished (less than or equal to 10 beats/min) variation of rate. The diminution in this variation was not related to the type or location of myocardial infarction, to maximum release of CK-MB or to cardiovascular medication. Our results suggest that impairment of vagal control of heart rate is common after myocardial infarction. The impairment cannot be predicted by any specific feature of the disease.

To evaluate the cardiovascular response to exercise in diabetes, a graded maximal exercise test was performed on 50 women with insulin-dependent diabetes mellitus, aged 15-40 years, and on 15 healthy women in the same age group. The diabetic subjects were divided into 3 groups according to the duration of disease: group 1: 0-5 years, group 2: 6-14 years, group 3: 15-29 years. The maximal work load was lower in the diabetic subjects than in the controls. The difference was most marked between the controls and group 3 (167 +/- 14 W vs 132 +/- 23 W, p less than 0.001). The maximal heart rate was lower in groups 2 and 3 than in the controls (173 +/- 16 vs 187 +/- 11, p less than 0.05). The diabetic women with long-standing disease had a slightly higher blood pressure response to exercise resulting in comparable rate-pressure products in the study groups. Two diabetic women in group 3 and one healthy woman had 1 mm ST depressions during the test without appearance of arrhythmias or chest pain. These studies suggest that exercise tolerance is reduced in young diabetic women, especially in patients with long-standing disease. The frequency of pathological exercise ECGs does not, however, seem to be increased.

The left ventricular (LV) response to isometric exercise was evaluated in 20 patients who performed handgrip exercise tests before and 3 months after coronary artery bypass grafting. Preoperative LV ejection fraction (EF) decreased during the handgrip test from 0.57 +/- 0.08 to 0.49 +/- 0.09 (p less than 0.001); the ratio between the LV peak systolic pressure (PSP) and end-systolic volume index (ESVI) did not change. In 12 patients with patent grafts, the LVEF after operation did not change (0.54 +/- 0.06 at rest and 0.56 +/- 0.06 during handgrip exercise) and PSP/ESVI ratio increased from 4.5 +/- 1.5 to 5.6 +/- 2.1 mm Hg/ml X m-2 (p less than 0.001) during exercise. In 8 patients with occluded grafts, the LVEF after operation decreased from 0.56 +/- 0.10 to 0.48 +/- 0.06 (p less than 0.02), whereas PSP/ESVI did not change during handgrip exercise. Thus, the LV response to isometric handgrip exercise appears to improve after coronary artery bypass grafting in patients with patent grafts, but not in patients with 1 or more occluded grafts.

To investigate the effects of different types of hemodialysis on hemodynamics, left ventricular size and function, 10 patients with uremia due to chronic renal failure were examined using echocardiography and measurement of systolic time intervals before and after both acetate and bicarbonate hemodialysis. Both caused decreases in left ventricular end diastolic (acetate -3.2 vs. bicarbonate -5.1 mm, p less than 0.01 for both) and end systolic (-3.2 vs. -3.7 mm, p less than 0.01 for both) diameters, and increases in mVCF (+0.24 vs. +0.23 circ/s, p less than 0.005 for both) and fractional shortening (+2.7%, p less than 0.05 vs. +0.9%, NS). In systolic time intervals, the LVETI decreased (-28 vs. -38 ms, p less than 0.001 for both) and the PEP/LVET ratio increased (+0.04, NS vs. 0.09, p less than 0.01). There were no significant differences between the changes in any of the measured parameters caused by acetate or bicarbonate hemodialysis, except in blood bicarbonate concentration (+1.9 vs. +5.4 mmol/l, difference p less than 0.01). Thus hemodialysis with acetate or bicarbonate base causes similar decreases in left ventricular size apparently because of decreased diastolic filling, but in spite of this, there is an increase in left ventricular systolic function, apparently partially due to increased myocardial contractility.