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Several investigators have shown signs of possible sympathetic but not parasympathetic reinnervation in heart transplanted patients. Spectral analysis of heart rate and blood pressure variability is a noninvasive tool appropriate to detect a functional autonomous reinnervation to the heart. In a follow-up study, 13 patients after heart transplantation (HTx) were investigated, mean age 50.6+/-8.5 years, 18 healthy volunteers were selected as control group. For each patient two recordings were performed which took part 14+/-5 months respectively 42+/-8 months after HTx. ECG and systolic blood pressure (SBP) have been recorded simultaneously for 5 min in supine position during controlled respiratory rate of 12 or 15 cycles/min. No graft rejection has been detected in the endomyocardial biopsy performed right after the recordings. Power spectral densities (PSD) were calculated for the beat-to-beat time series of RR-intervals (distance of two following QRS complexes) and SBPs. The area of PSD in the range of 0.05-0.17 Hz was defined as low frequency (LF) and that of 0.18-0.35 Hz as high frequency (HF). LF and HF are indicative of efferent sympathetic respectively parasympathetic activity at the sinus node. A significant increase of LF (226%) and HF (213%) during a mean period of 28 months could be found. No differences were to be shown for systolic blood pressure variability. Previous findings confirm that LF band increases 4 years after transplantation, suggesting a possible sympathetic reinnervation of the heart. On the other hand an increase of the HF band also suggests a parasympathetic reinnervation.

Background: In several angiographic trials, HMG-CoA reductase inhibitors have shown a beneficial effect on the progression of coronary artery disease. Using 20 mg simvastatin, day-1, a treatment period of up to 4 years was necessary to show a significant reduction in coronary artery disease progression. The question remains however whether higher dosages of simvastatin would be more advantageous in respect to the magnitude of the effect and the required time interval to demonstrate treatment efficacy., Methods and Results: In the Coronary Intervention Study (CIS), a multicentre randomized double-blind placebo-controlled study, the effects of lipid-lowering therapy with simvastatin on progression of coronary artery disease in 254 men with documented coronary artery disease and hypercholesterolaemia were investigated. Following a period of lipid-lowering diet, treatment with 40 mg simvastatin or placebo was maintained for an average of 2.3 years. Two primary angiographic endpoints were chosen: the global change score (visual evaluation according to the method of Blankenhorn) and the per patient mean change of minimum lumen diameter (evaluated by the CAAS I system). The mean simvastatin dose was 34.5 mg day-1. In the placebo group, the serum lipids remained unchanged; in comparison to the placebo group the simvastatin group showed a 35% LDL-cholesterol decrease. Coronary angiography was repeated in 205 patients (81%) and 203 film pairs (80%,) were evaluable by quantitative coronary angiography. In the simvastatin and placebo groups, the mean global change scores were +0.20 and +0.58 respectively, demonstrating a significantly slower progression of coronary artery disease in the treatment group (P = 0.02). The change in minimum lumen diameter assessed by computer-assisted quantitative evaluation with the CAAS I system was -0.02 mm in the simvastatin group and -0.10 mm in the placebo group (P = 0.002). In the simvastatin group, there was a significant correlation between the LDL cholesterol levels achieved therapeutically and the per patient mean loss of minimum lumen diameter (r = 0.29; P = 0.003). During the study period, there was no significant difference in the incidence of serious cardiac events (15 of 129 patients in the simvastatin group and 19 of 125 patients in the placebo group, ns)., Conclusion: Treatment with 40 mg simvastatin day-1 reduces serum cholesterol and slows the progression of coronary artery disease significantly within a short period of treatment time. In the treatment group, retardation of progression is inversely correlated to the LDL-cholesterol levels achieved.

Method: In exercise training with chronic heart failure patients, working muscles should be stressed with high intensity stimuli without causing cardiac overstraining. This is possible using interval method exercise. In this study, three interval exercise modes with different ratios of work/ recovery phases (30/60 s, 15/60 s and 10/60 s) and different work rates were compared during cycle ergometer exercise in heart failure patients. Work rate for the three interval modes was 50% (30/60 s), 70% (15/60 s) and 80% (10/60 s) of the maximum achieved during a steep ramp test (increments of 25 w/10 s) corresponding to 71, 98 and 111 watts on average. Metabolic and cardiac responses to the three interval exercises were then examined including catecholamine levels and perceived exertion. Parameters measured during interval exercise were compared with an intensity level of 75% peak VO2, determined during an ordinary ramp exercise test (increments of 12.5 W.min-1)., Results: (mean +/- SEM) (1) In all three interval modes, VO2, ventilation and lactate did not increase significantly during the course of exercise. Mean values during the last work phase were between 754 +/- 30 and 803 +/- 46 ml.min-1 for VO2, between 26 +/- 3 and 28 +/- 1 l.min-1 for ventilation and between 1.24 +/- 0.14 and 1.29 +/- 0.10 mmol.l-1 for lactate. (2) In mode 10/60 s, heart rate and systolic blood pressure increased significantly (82 +/- 4 --> 85 +/- 4 beats.min-1; 124 +/- 5 --> 134 +/- 5 mmHg; P < 0.05 each), while in mode 15/60 s catecholamines increased significantly (norepinephrine 0.804 +/- 0.089 --> 1.135 +/- 0.094 nmol.l-1; P < 0.008; epinephrine 0.136 +/- 0.012 --> 0.193 +/- 0.019 nmol.l-1; P < 0.005). (3) In all three modes, rating of leg fatigue and dyspnoea increased significantly during exercise but remained within the range of values considered 'very light to fairly light' on the Borg scale. (4) Compared to an intensity level of 75% peak VO2, work rate during interval work phases was between 143 and 221%, while cardiac stress (rate-pressure product) was significantly lower (83-88%)., Conclusion: All three interval modes resulted in physical response in an acceptable range of values, and thus can be recommended.

Unlabelled: The study was carried out to determine the relationship between ventilatory threshold and the onset of ischaemia, as shown on the ECG (horizontal and/or descending ST depression of 0.05 mV, on average). Twenty-seven male patients (aged 58 +/- 7 years) with angiographically documented coronary artery disease (CAD) were assessed by cardiopulmonary exercise testing without medication. Oxygen uptake (VO2), heart rate (HR), rate-pressure-product (RPP) and blood lactate were measured and/or calculated every 30 s during exercise. In addition, 10 patients, comparable with the above group, were examined to find out the acute effects of isosorbide dinitrate (ISDN) at ventilatory threshold in relation to ischaemic threshold. The first cardiopulmonary exercise test was carried out without medication, the second 1 h later with 5 mg ISDN, taken sublingually 30 min before the test., Results: (means, SD): (1) The mean ventilatory threshold preceded the ischaemic threshold in relation to exercise capacity (48 +/- 14 vs 55 +/- 20 watts; P < 0.05), VO2.kg-1 (10.0 +/- 2.2 vs 12.0 +/- 2.9 ml.kg-1.min; P < 0.05), HR (93 +/- 15 vs 100 +/- 16.min-1; P < 0.01), RPP (15095 +/- 4424 vs 17166 +/- 5245; P < 0.01) and blood lactate (1.28 +/- 0.53 vs 1.44 +/- 0.60 mmol.l-1; P < 0.05). (2) This relationship was observed more often in the subgroup of patients with angina during cardiopulmonary exercise testing or with myocardial infarction or with three-vessel disease than in patients without angina or infarction or with one- and two-vessel disease.(ABSTRACT TRUNCATED AT 250 WORDS)

The goal of this study was to assess the current practice of endocarditis prophylaxis in Germany. We conducted a survey using a standardized questionnaire, which was sent to 100 hospital cardiologists, to 430 cardiologists in office practice and to 389 dentists and oral surgeons. In addition, 364 patients with valvular or congenital heart disease were interviewed in our outpatient clinic. Seventy five percent of cardiologists informed their patients by both written and oral instructions. Half recommended the use of penicillin, according to the German Society of Cardiology, while the rest followed recommendations of other societies. Sixty-three percent of patients who had undergone a procedure requiring prophylaxis against bacterial endocarditis within the year prior to the questionnaire, had actually received it. This is higher than previously reported, but is far from acceptable. The indications for prevention of endocarditis, as seen by the dentists, deviated markedly from official recommendations. Although 77% administered antibiotics themselves, in only 57% did the type of prophylaxis applied correspond to one of the available recommendations. Recommendations on the prevention of bacterial endocarditis are not well known dentists and oral surgeons who perform procedures for which it is indicated. Further patient- and physician-oriented strategies are urgently needed to improve compliance with prevention of endocarditis in Germany.

The acute and short-term effects of treatment with 10 consecutive doses of isosorbide dinitrate 40 mg t.i.d. and molsidomine 8 mg t.i.d. in slow release formulations were investigated in 10 patients with angiographically documented coronary artery disease and stable angina pectoris according to a randomized, double-blind, double-dummy, cross-over study design using conventional symptom-limited exercise testing. Acute exercise testing 3 h following the first dose of ISDN and molsidomine showed a significant reduction of maximal ST segment depression and of the area above the ST segments. Time to occurrence of 0.1 mV ST segment depression, exercise duration, time to onset of angina and exercise tolerance increased significantly. On the fourth treatment day with ISDN and molsidomine an attenuation of these antiischaemic effects was seen. The mean effects on ST segment depression, area above ST segments, time to occurrence of 0.1 mV ST segment depression, exercise duration, time to onset of angina and exercise tolerance were reduced by 40%, 44%, 47%, 58%, 54% and 65%, respectively, in patients administered ISDN and by 33%, 48%, 58%, 59%, 45% and 60% in those given molsidomine. Thus, following sustained short-term therapy the antiischaemic effects of both drugs seem to be attenuated. In this report no marked differences were found between ISDN and molsidomine.

Six levels of coronary pain are defined and for each of them explanations for absence of pain in asymptomatic myocardial ischaemia are given: Level I: Myocardial ischaemia which can be less pronounced in amount during asymptomatic episodes. Level II: Adequate stimulus (chemical, mechanical) where biosynthesis of algogesic substances, degree of local mechanical involvement and spatial distribution may be different. Level III: For neuronal encoding the intensity theory is mainly for coronary pain, presupposing a central pain threshold which is higher in asymptomatic patients. Level IV: Conduction of painful information may be interrupted by destruction of afferent nerve ways. Level V: Spinal transmission: resting tone and ability to activate neural and humoral (endorphinergic) pain inhibition systems are stronger in asymptomatic patients. Level VI: Central processing: cognitive mechanisms (coping style) affect perception of coronary pain with differences in symptomatic and silent myocardial ischaemia.

In a double-blind study, eight patients with symptomatic myocardial ischaemia and nine with asymptomatic myocardial ischaemia were compared during physical exercise under naloxone (6 mg i.v.) or placebo. Plasma beta-endorphin, cortisol and catecholamines were measured before exercise, during maximal exercise, and 10, 20 and 60 min after exercise. A tourniquet pain test (on the forearm, under control of transcutaneous PO2), and an electrical pain test (intracutaneous electrode placed in the finger with the electrical stimulus under computer control and two-interval forced-choice psychophysical technique) were performed before exercise as well as immediately after, and 60 min after exercise. Plasma beta-endorphin levels increased significantly (P less than 0.01) during exercise in symptomatic and asymptomatic patient groups; every patient showed an increase on beta-endorphins during and after exercise. However, the increase found in beta-endorphins during and after exercise was significantly larger (P less than 0.01) in asymptomatic than in symptomatic patients. After naloxone, this difference was no longer evident. Angina pectoris during exercise was reported with less latency in symptomatic patients (P less than 0.05) and occurred in two of nine asymptomatic patients following naloxone. The time course of plasma cortisol levels exhibited the same pattern as beta-endorphins with the same significant differences between symptomatic and asymptomatic groups. Electrical pain thresholds, though on average higher in asymptomatic patients (2.21 mA vs. 0.79 mA), were not affected by exercise or naloxone. Asymptomatic patients required more time to reach pain thresholds in the tourniquet pain test (P less than 0.02). After exercise, tourniquet pain thresholds were significantly lower (P less than 0.01) under naloxone compared with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

To evaluate the influence of PTCA on symptomatic and asymptomatic ischaemic episodes in 94 patients, 24-h ambulatory, electrocardiographic Holter recordings were obtained before and after successful PTCA. Sixty-four per cent of patients had one-vessel disease, 28% two-vessel disease and 8% had three-vessel disease. Ischaemic episodes were present in 36% of patients before PTCA, of which 71% were silent; after PTCA, 23% of patients had ischaemic episodes, of which 98% were silent; thus silent ischaemic episodes were improved by PTCA to a lesser degree than symptomatic ischaemic episodes. Successful PTCA lead to a significant reduction in total number and duration of ischaemic episodes but not to a complete abolition. Patients with silent ischaemic episodes after PTCA had also a higher incidence of silent ischaemic episodes before PTCA. Functional and haemodynamic improvement was comparable in patients with and without silent ischaemic episodes. No specific cause for the persistent or newly appearing silent ischaemic episodes after PTCA could be identified; they are not indicative of an inadequate dilatation and cannot be considered as a risk factor for early restenosis. A possible explanation could be a traumatically induced, increased vascular tone in susceptible patients.

Assessment of prognosis plays an important role in the management of patients with CAD. The objective of the study was to improve risk stratification in patients with known coronary angiographic findings. We analyzed the prognostic importance of 13 angiographic, exercise, and clinical variables in 1183 medically treated patients with documented CAD. Five-year actuarial survival rate (5-YSR) was 87%. Multivariate analysis with the proportional hazards regression model revealed four continuous and one discrete variable to be of independent prognostic importance (chi 2 value): cardiac output at the highest work load (COmax) (chi 2 = 80.7); coronary score (chi 2 = 18.6); heart volume by X-ray (chi 2 = 14.7); maximal pulmonary wedge pressure during exercise (chi 2 = 5.3), and history of myocardial infarction (chi 2 = 4.8). Inclusion of these variables in the survival function according to the regression model resulted in excellent prediction of 5-YSR, e.g. in the patients with three-vessel disease (N = 399): actuarial 5-YSR was 80%, calculated 81%. Patients with three-vessel disease and COmax greater than 11.21 min-1 (N = 188) had an actuarial 5-YSR of 88%, calculated 89%; if COmax was less than 11.21 min-1 the actuarial 5-YSR was 71%, calculated 70%. Patients with three-vessel disease from an independent cohort of surgically treated patients (N = 507) had a calculated 5-YSR under an assumed medical regimen of 77%.(ABSTRACT TRUNCATED AT 250 WORDS)

Nowadays, the majority of patients undergoing aortocoronary bypass surgery have a history of myocardial infarction. In our first series of 1000 patients operated between 1973 and 1979, about two thirds of the patients had suffered myocardial infarction; about 80% of them within the previous three months. The method most frequently used to select post-infarction patients for coronary angiography is a simple exercise test. The post-infarction period in the context of this symposium was defined as the first 12 weeks after infarction. As far as exercise tests are concerned, we may divide this period into three subperiods: the very early post-infarction period, especially the first week after infarction. Exercise testing does not play a role in this very early period; the second period is the time of an early post-infarction exercise test or the predischarge exercise test (second and third week); from the fourth to the twelfth week in many European countries, rehabilitation measures will follow, usually in a special institution. This is the time of what we will call in short 'the late post-infarction exercise test'.

ST segment monitoring by Holter ECG was conducted in 80 consecutive patients 2-4 weeks before aortocoronary bypass surgery and three weeks and six months after surgery. Preoperatively, all patients were under maximal medical therapy. In 31 out of 80 patients medical therapy could be stopped and thus 24-h ST monitoring could also be conducted without medication. Preoperative and early postoperative (three weeks) examinations were performed under hospital conditions. At 6 months after surgery the patients were monitored at home during their everyday activities. Twenty-eight per cent of patients waiting for aortocoronary bypass surgery under full medication showed transient ischaemic episodes in 24-h Holter ECG. Seventy-eight per cent of these episodes were asymptomatic. Without medication, 55% of patients had transient ischaemia. The exercise ECG data partly predicted the Holter ECG data. Patients with ST segment depression greater than 0.1 mV during exercise ECG had on Holter monitoring more and longer lasting ischaemic episodes than those with ST segment depression less than or equal to 0.1 mV. In patients with asymptomatic ST segment depression during exercise ECG the relation of silent episodes to symptomatic episodes on Holter monitoring was 5.3:1 while in patients with symptomatic ST segment depression during exercise ECG this relation was 2.3:1. Three weeks after operation the informative value of the Holter ECG was very restricted due to changes in the resting ECG caused by the operation and because patients do not exert themselves much at this time. Six months after surgery, Holter ECG is more informative, especially when conducted at home.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise-induced ST-segment depression is a marker of impaired prognosis in patients with suspected or manifest CAD. Whether ST-segment depression remains of prognostic importance, after exercise tolerance and extent of CAD have been considered, is unknown. We analysed the prognostic importance of exercise-induced ST-segment depression (greater than 0.15 mV) in 1250 medically treated patients with angiographically determined CAD (mean follow-up after angiography 4.5 years). Based on exercise tolerance (supine bicycle ergometry) patients were divided into two groups: group A patients (n = 677) with lower exercise tolerance (less than or equal to 75 W) and group B patients (n = 573) with better exercise tolerance (greater than 75 W). Group A patients had a lower 5-year survival rate than group B patients (81.5% versus 94%, P less than 0.00001). In group A, patients with ST-segment depression had a lower 5-year survival rate than patients without ST-segment depression (76% versus 85%, P = 0.01). In group B, patients with and without ST-segment depression had similar 5-year survival rates (90% versus 96%, P = 0.11). Subgroup analysis of groups A and B according to number of diseased vessels and presence or absence of ST-segment depression revealed that exercise-induced ST-segment depression (greater than 0.15 mV) was of additional prognostic importance only in patients with triple vessel disease. 5-year survival rates in group A with triple vessel disease were 71% with and 80% (P = 0.057) without ST-segment depression.(ABSTRACT TRUNCATED AT 250 WORDS)

Quantification of heart failure is possible with hemodynamic parameters such as cardiac output and filling pressure at rest and during exercise. These parameters can easily but invasively be achieved by floating catheter measurements. In our experience, the risk of this method is low but existent. In greater than 20 000 patients with chronic diseases no death occurred in connection with the procedure; 26 patients developed ventricular fibrillation or ventricular tachycardias which made defibrillation necessary in 10 of these patients. In three patients asystolia demanded resuscitation. Hemoptysis did not occur. In the acute stage of a disease, e.g. in the acute myocardial infarction, the risk may be higher, especially if the catheter remains in the circulation for longer periods. The possibilities and limitations of the method will be discussed for the following patient groups: (1) Patients with acute myocardial infarction, (2) Postinfarction patients, (3) Patients with cardiomyopathies, (4) Patients with valvular heart disease.