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Thirteen patients with chronic renal failure and uraemia were investigated by echocardiography preoperatively before and after haemodialysis and again after a successful renal transplantation to evaluate the cardiac changes caused by renal transplantation. After renal transplantation, the left ventricular end-diastolic and end-systolic diameters, as well as the cardiac index, decreased, probably because of the decreased left ventricular filling pressure. The left ventricular wall thickness and mass decreased, apparently as a result of the decrease of the left ventricular preload and also of the decrease of the afterload, because the systolic blood pressure decreased. The left atrial diameter decreased in response to the decreased left ventricular preload and wall hypertrophy. The changes in the indices of left ventricular function as a result of haemodialysis appeared to predict the changes seen after renal transplantation. Renal transplantation appears to have a tendency to result in normal left ventricular and left atrial volumes, as well as to lessen left ventricular hypertrophy, without significantly improving left ventricular function. [ABSTRACT FROM PUBLISHER]

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 efficacy of amiodarone has been proved in long-term maintenance of sinus rhythm (SR) in patients with paroxysmal atrial fibrillation (AF). The present study evaluates the efficacy and safety of a single oral dose of amiodarone in patients with recent-onset AF (<48 hours). Seventy-two patients were randomized to receive 30 mg/kg of either amiodarone or placebo. Conversion to SR was verified by 24-hour Holter monitoring. Ten patients were excluded because of SR in the beginning of monitoring or technical failure during Holter monitoring. The remaining study groups were comparable (n = 31 for each), except that in the placebo group beta blockers were more common. The patients receiving amiodarone converted to SR more effectively than those receiving placebo (p<0.0001). At 8 hours, approximately 50% of patients in the amiodarone group and 20% in the placebo group (Holter successful) had converted to SR, whereas after 24 hours the corresponding figures were 87% and 35%, respectively. The median time for conversion (8.7 hours for amiodarone and 7.9 hours for placebo) did not differ in the groups. Amiodarone was hemodynamically well tolerated, and the number of adverse events in the study groups was similar. Amiodarone as a single oral dose of 30 mg/kg appears to be effective and safe in patients with recent-onset AF. [ABSTRACT FROM AUTHOR]

Aortic valve lesions are often found in patients with rheumatic diseases, but their clinical significance has not been properly evaluated. In the present study, the echocardiographic files of the cardiology unit of the Oulu University Hospital were screened for a diagnosis of aortic insufficiency (AI). The aetiology of the valve disease and specific details of the rheumatic disease were evaluated in 160 patients. Twenty-eight patients (18%) had a history of rheumatic fever. Rheumatic disease was found in 14 patients (8.8%) with AI, which is significantly more than the prevalence of rheumatic diseases (1.8%) in the corresponding age group (35-100 years) in Finland. Rheumatoid arthritis or juvenile rheumatoid arthritis was found in seven patients (4.4%), whereas ankylosing spondylitis or seronegative spondylarthropathy were found in four patients (2.5%). Other rheumatic diseases included Takayasu's arteritis (two patients) and scleroderma (one patient). When 38 patients with pure AI without other possible aetiology were analysed, rheumatic disease was found in five patients (13%). Patients with rheumatic disease as a potential aetiology of AI often had symptomatic valve disease, which required surgical treatment, although great differences between different aetiologies were not found.

Background: Hypertension is associated with changes in concentrations of vasoactive peptides and procollagen propeptides, but their relationships with left ventricular hypertrophy and cardiac function are unclear., Methods: We measured plasma levels of atrial natriuretic peptide (ANP), its amino terminal propeptide (NT-proANP), B-type natriuretic peptide (BNP), endothelin-1 (ET-1), and serum levels of the aminoterminal propeptide of type I procollagen (PINP) and the aminoterminal propeptide of type III procollagen (PIIINP) and echocardiographic parameters in 97 patients with hypertension in the Anglo-Scandinavian Cardiac Outcomes Trial., Results: Median values (reference values) of the peptides were: ANP 11.2 (6.9-14.9) pmol/l, NT-proANP 351 (143-311) pmol/l, BNP 1.1 (0.4-7.2) pmol/l, ET-1 8.7 (1.2-5.0) pmol/l, PIIINP 2.8 (1.7-4.2) microg/l and PINP 29 (19-84) microg/l. Plasma BNP levels in patients with left ventricular hypertrophy (1.2 pmol/l) and patients with echocardiographic signs of diastolic dysfunction (1.5 pmol/l) were greater than those in patients without hypertrophy (0.7 pmol/l) and normal diastolic parameters (0.9 pmol/l) (p<0.05). BNP was the only biochemical parameter that independently predicted interventricular septal diastolic diameter (p<0.05), left ventricular mass index (p<0.01) and ratio of the velocity-time integrals of the E and A waves of the mitral inflow in a stepwise logistic regression analysis (p<0.05)., Conclusions: The results show that BNP reflects the remodelling process in hypertension.

Background: The risk of early sudden death before hospital admission is higher in diabetic than non-diabetic men with acute myocardial infarction and autonomic nervous activity may modify the clinical outcome of abrupt coronary occlusion. Since diabetes mellitus may interfere with autonomic and myocardial function, we decided to study whether diabetes alters autonomic and haemodynamic responses to acute coronary occlusion., Methods: We analyzed the changes in heart rate, heart rate variability and blood pressure, and the occurrence of ventricular ectopy during a 2-min coronary occlusion in 238 non-diabetic and 32 diabetic patients referred for single vessel coronary angioplasty. The ranges of non-specific responses were determined by analyzing a control group of 19 patients with no ischaemia during a 2-min balloon inflation in a totally occluded coronary artery., Results: Diabetic patients were more often (p<0.05) female, but there were no significant differences in the occluded vessel or incidence of ST changes or chest pain during coronary occlusion between the groups. Incidence of significant heart rate reactions and ventricular arrhythmias was comparable in both groups. Systolic blood pressure decreased (p=0.01) in the diabetic patients during coronary occlusion, but did not change significantly in the non-diabetic group. Coronary occlusion caused more often (34% vs. 14%, p<0.01) a significant decrease in blood pressure in diabetic patients. Logistic regression models developed to analyze the significance of diabetes while controlling for baseline variables and signs of ischaemia identified diabetes to be an independent predictor of hypotensive reactions (odds ratio [OR] 2.9, 95% confidence intervals 1.1-7.8, p<0.05), while female gender and high short-term heart rate variability were other independent predictors of hypotensive reactions., Conclusions: Diabetic patients often develop significant hypotension during the early phase of acute coronary occlusion. This abnormality may be related to diabetic cardiomyopathy and impairment of baroreflex-mediated regulation of circulation. Predisposition to hypotension may contribute to the observed differences in the clinical presentation and outcome of acute coronary events.

Lipoprotein(a) [Lp(a)] is an important risk factor for cardiovascular disease. Alcohol is one of the few nongenetic factors that lower Lp(a) levels, but the metabolic mechanisms of this action are unknown. Alcohol inhibits the growth hormone (GH)/insulin-like growth factor-I (IGF-I) axis. Alcohol might also affect IGF-binding protein-1 (IGFBP-1), which is an acute inhibitor of IGF-I. We studied how alcohol withdrawal affects Lp(a) levels and the GH/IGF-I/IGFBP-1 axis. Male alcohol abusers (n=27; 20 to 64 years old) were monitored immediately after alcohol withdrawal for 4 days. Twenty-six healthy men, mainly moderate drinkers, served as control subjects. Fasting blood samples were drawn to determine Lp(a), IGF-I, and IGFBP-1 (by ELISA, RIA, and immunoenzymometric assay, respectively). Nocturnal (12 hours) urine collection was performed in 9 alcoholics and 11 control subjects for GH analyses (RIA). The groups were similar in age and body mass index. Lp(a), GH, and IGF-I tended to be lower and IGFBP-1 higher in the alcoholics immediately after alcohol withdrawal than in the control subjects. During the 4-day observation in alcoholics, Lp(a) levels increased by 64% and IGF-I levels by 41%, whereas IGFBP-1 levels decreased by 59% (P<.001 after ANOVA for all comparisons). Urinary GH levels tended to decline. The increase in Lp(a) correlated inversely with the changes in IGFBP-1 (r= -.63, P<.001, n=27) and GH (r=-.70, P<.05, n=9), but not with IGF-I. In multiple regression analysis, the main predictors for the increase in Lp(a) were IGFBP-1 and urinary GH. In conclusion, alcohol withdrawal induces interrelated and potentially atherogenic changes in Lp(a) and IGFBP-1 levels.

Objectives: We sought to determine whether there are gender-related differences in autonomic and hemodynamic responses to abrupt coronary occlusion., Background: The risk of sudden death before hospital admission is higher in men with an acute myocardial infarction. The reasons for this gender-related difference are not well understood. Cardiovascular autonomic regulation modifies the outcome of acute coronary events, and there are gender differences in the autonomic regulation of heart rate (HR) in normal physiologic circumstances., Methods: We analyzed the changes in HR, HR variability and blood pressure and the occurrence of ventricular ectopic beats during a 2-min coronary occlusion in 140 men and 65 women referred for single-vessel coronary angioplasty. The ranges of nonspecific responses were determined by analyzing a control group of 19 patients with no ischemia during a 2-min balloon inflation in a totally occluded coronary artery., Results: Women more often had ST segment changes (p < 0.01) and chest pain (p < 0.05) during the occlusion. Significant bradycardia or increase in HR variability as a sign of vagal activation occurred more often in women than in men (31% vs. 13%, p < 0.01 and 25% vs. 11%, p < 0.05, respectively). Coronary occlusion also more often caused (28% vs. 11%, p < 0.01) a decrease in blood pressure in women. The most pronounced female preponderance was in the incidence of Bezold-Jarisch-type reaction (i.e., simultaneous bradycardia and decrease in blood pressure [16% vs. 0.7%, p < 0.0001]). Logistic regression models developed to analyze the significance of gender while controlling for baseline variables and signs of ischemia identified female gender to be an independent predictor of bradycardic reactions (odds ratio [OR] 3.2, 95% confidence interval [CI] 1.4 to 7.7, p < 0.01), hypotensive reactions (OR 2.6, 95% CI 1.1 to 6.0, p < 0.05) and Bezold-Jarisch-type response (OR 22.2, 95% CI 2.5 to 200, p < 0.01). Significance of female gender as a protector against early coronary occlusion-induced ventricular ectopic beats emerged as having borderline significance (OR 0.4, CI 0.1 to 1.1, p = 0.07)., Conclusions: Vagal activation is more common in women than in men during abrupt coronary occlusion and may have beneficial antiarrhythmic effects, modifying the outcome of acute coronary events.

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.

Ventriculoatrial (VA) sequence and neurohumoral responses may be important modulators of hemodynamic recovery during VT. We studied the effects of VA conduction on blood pressure recovery, and levels of atrial natriuretic peptide (ANP), epinephrine, and norepinephrine during simulated VT. After diagnostic coronary angiography, VT was simulated by rapid right ventricular pacing (150 beats/min, 3 mins) in a consecutive series of patients. Whenever the patients demonstrated VA dissociation during ventricular pacing, they were included in the study. After 10 minutes of recovery, a group of nine patients then underwent an additional VA pacing (150 beats/min, 3 mins, VA delay of 150 msec). Intra-arterial blood pressure was continuously monitored, and plasma ANP and catecholamine levels were measured before, during, and after both pacing protocols. The mean arterial pressures declined rapidly by 26% and 30% after initiation of ventricular and VA pacing, respectively. The blood pressure then gradually recovered, the hemodynamic recovery being better during VA pacing. Plasma ANP and catecholamine levels increased toward the end of both pacing periods. The observed increase in ANP concentration was more prominent during VA pacing than ventricular pacing (P < 0.001), whereas catecholamine levels increased similarly. The results show that during simulated VT hemodynamic recovery is partially dependent on VA sequence. The increases in circulating ANP and catecholamines occur too slowly to account for the rapid changes in blood pressures observed after initiation of simulated VT. Therefore, other mechanisms, such as reflex stimulation of the sympathoadrenergic nervous system, must be involved, too. ANP release increases when atrial contraction frequency increases, but the exact determinants for this release remain unknown.

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)

Myocardial ischemia, electrolyte changes, and fluctuations in autonomic tone may play an important role in the presentation of malignant ventricular arrhythmias. beta-Adrenoceptor blocking agents have been shown to decrease the incidence of ventricular fibrillation and sudden cardiac death in patients with coronary artery disease. Therefore we investigated the changes in myocardial metabolism and transcardiac electrolytes during simulated ventricular tachycardia before and after beta-adrenergic blockade. Six patients with normal coronary arteries (group 1) and 12 patients with documented coronary artery disease (group 2) were included in the study. The right ventricle was paced with electrode catheters to a constant cycle length of 400 msec for 3 minutes. Blood samples were withdrawn simultaneously from the coronary sinus and femoral artery to determine the transcardiac differences in metabolic variables and electrolytes before the pacing, at the end of the pacing, and 2 minutes thereafter. After pacing, the patients were given intravenous propranolol (0.15 mg/kg), and the protocol was repeated. Intraarterial blood pressure and electrocardiogram were monitored continuously. There was a rapid decline of the mean arterial blood pressures after initiation of the pacing in both study groups, whereafter the pressures began to rise. Propranolol somewhat blunted the blood pressure recovery, especially in group 2. Norepinephrine levels increased during the pacing in both patient groups, and the increase was accentuated by beta-adrenergic blockade. The femoroarterial coronary sinus difference in lactate turned negative, and pH, PCO2 and potassium differences increased in group 2 during pacing. However, the myocardial energy state remained relatively good as estimated from the nonsignificant change in the transcardiac differences of the plasma adenosine catabolites. There were no changes in the metabolic variables or transcardiac electrolytes in group 1 patients during pacing. Propranolol did not prevent the metabolic ischemia, but it did prevent the pacing-induced decrease in coronary sinus potassium and increase in transcardiac potassium difference. Propranolol also decreased arterial levels of free fatty acids and their extraction in group 2 patients during pacing. In conclusion, blood pressure decay during simulated ventricular tachycardia is followed by instantaneous sympathoadrenergic activation. In patients with coronary artery disease, this process is accompanied by metabolic ischemia and net transfer of extracellular potassium into the intracellular space. The metabolic and electrolyte changes may result in alterations of electrophysiologic millieau, thereby also modifying the clinical characteristics of ventricular tachycardia. Propranolol decreases arterial levels of free fatty acids and prevents changes in transcardiac electrolytes observed in coronary artery disease patients during simulated ventricular tachycardia. These effects of propranolol may be of clinical significance.