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Objectives: Prognosis and course of severe left ventricular dysfunction have been shown to be influenced positively by exercise training. Yet, physicians have been reluctant to include exercise into therapeutic concepts due to widespread uncertainty about the acceptable intensity of cardiac stress. Standardized exercise programs with proven safety may promote acceptance of this approach., Patients and Methods: 25 patients with severe heart failure were enrolled in a PC-controlled interval exercise training on cycle ergometer, lasting 21 minutes five times a week for a 4-week inpatient period. After discharge patients performed incremental daily walking for 3 months. Associated educational measures concerned life-style changing and self-controls., Results: None of the patients had to interrupt the training because of side effects. 3 weeks and 3 months after starting exercise training there was an increase of peak VO2 from 13.4 +/- 2.8 to 14.5 +/- 3.8 (p < 0.05) and 15.3 +/- 3.2 ml/kg/min (p < 0.01), respectively, and an increase of ventilatory anaerobic threshold (VAT) from 9.3 +/- 1.9 to 10.0 +/- 2.3 (p < 0.05) and 11.3 +/- 2.2 ml/kg/min (p < 0.001), respectively. The improved aerobic capacity corresponded to a 9.3% increase in the results of the 6-minute walk test in the 4th week (n.s.). During out-patient period, the walking could be increased from 37 to 58 minutes daily. The physical quality of life was significantly improved after 3 months. There was no hospital admission due to heart failure., Conclusion: Exercise training in the therapy of severe heart failure is safe and increases the aerobic capacity. Associated educational measures may be able to minimize the danger of wrong exercise techniques and to reduce the rate of hospital readmissions.

Traditional concepts about the early phase of postoperative remobilization after cardiac surgery favor physical inactivity--as did earlier concepts for rehabilitation after myocardial infarction like the armchair treatment philosophy. For an overwhelming majority of our patients, however, this concept does not hold, according to our experience during the last decade. In contrast, we propose a model of stepwise mobilization and rehabilitation starting the first postoperative days. At the end of the first week most patients are able to climb staircases. In the second week group physical therapy can be started. At the 14th postoperative day, discharge from the surgical ward is warranted. During this step of early mobilization some exceptions have to be made and some special aspects have to be considered. Early mobilization must be postponed in patients with overt heart insufficiency, a low ejection fraction, complex ventricular arrhythmias or pericardial effusions. Cautious mobilization is also required in patients with mitral valve replacement and persistent elevation of pulmonary pressure and resistance. This holds also for patients with valve replacement during acute endocarditis, patients with repair of a dissecting aneurysm of the aorta and patients with perioperative myocardial infarction. The stage of early postoperative mobilization usually ends after the second week and is followed by the next step, the rehabilitation phase during weeks 3 to 6. The goals of the rehabilitation program are; increasing the physical fitness of the patient, thereby increasing his self-assurance and self-esteem; establishing a health-education program, increasing the patients health competence and his coping capacities.(ABSTRACT TRUNCATED AT 250 WORDS)

Thirty-two hospitalized patients with angiographically-documented coronary artery disease and stable angina pectoris (NYHA class III) were randomly assigned to one of four treatment groups. After a one-week washout period, baseline examinations (systolic time intervals, blood pressure and exercise ECG) were performed. The patients were then treated with either 20 mg isosorbide dinitrate in sustained-release form (sustained-release ISDN), 20 mg isosorbide 5-mononitrate (IS 5-MN), 2.5 mg buccal nitroglycerin in sustained-release form (NTGB) or 6.5 mg oral nitroglycerin in sustained-release form (NTGO) and one hour thereafter, the heart rate, blood pressure and systolic time intervals were determined. Subsequently, the patients were treated with the respective nitrates four times daily for two weeks. On the seventh and 14th days, the heart rate, blood pressure and systolic time intervals were again determined before and after the first dose of the day. Additionally, after the first dose on the 14th day, an exercise ECG was performed. The effect of the nitrates on the venous capacitance system is reflected by the increase in the PEP/LVET ratio where NTGO and NTGB elicited marked actions and those of sustained-release ISDN and IS 5-MN were of a lesser extent. An effect on systolic and diastolic blood pressure at rest and during exercise could be documented only after administration of NTGB. The anti-ischemic effect of the nitrates was based on the reduction of ST-segment depression during exercise; after two weeks of treatment, sustained-release ISDN and IS 5-MN were associated with complete tolerance development while NTGO continued to exert a slight, and NTGB a clear reduction in ST-segment depression. Personal protocols documented that nitrate consumption and rate of anginal attacks during longterm treatment were unaffected by sustained-release ISDN, IS 5-MN and NTGO, but were reduced by 50% while on treatment with NTGB.

66 patients with 2 and 3 vessel coronary heart disease were studied before and after complete successful revascularization. Hemodynamic measurements and biplane left ventricular angiograms were obtained at rest and during supine bicycle exercise.--After operation a significant overall decrease of LVEDP with exercise was seen; exercise LVEF increased in cases with left main disease and in most cases with double vessel disease and double bypass. Inconsistant response was present in 3 vessel disease. Improvement of left ventricular dynamics with exercise in advanced coronary disease after complete revascularization can be expected mainly in 2 vessel disease and left main coronary disease.

The effects of atrial pacing and dynamic exercise in the supine position on systolic time intervals (STI) were compared in 10 normals. In another group of 13 normals, the effect of exercise alone on STI was tested. A linear shortening of electromechanical systole (QS2) and left ventricular ejection time (LVET) with increasing heart rate was demonstrated with right atrial pacing and dynamic exercise in the frequency range between 60 and 140 beats/min. However, the shortening of LVET was significantly less (p less than 0.01) with exercise compared to pacing. This is explained by an increase in left ventricular stroke volume with exercise. The preejection period (PEP) was significantly (p less than 0.001) shortened with exercise, but there was no change with atrial pacing. Thus, changes in heart rate (HR) alone, without changes in the dynamic state of the heart, did not influence PEP. It is suggested that PEP at rest should not be corrected for heart rate. The supine exercise regression equations for correction of heart rate for LVET and PEP differ from both the resting and the upright exercise regression equations. With exercise a frequency correction of STI using regression equations should be abandoned. Instead, uncorrected STI at standard heart rates (e.g., 100, 110, and 130 beats/min) should be taken for comparison. Heart rate standardization should be employed using the formula: Formula (See Text).

In a 47-year-old man suffering from sick-sinus syndrome the sinus node recovery time was determined. During rapid atrial stimulation a supraventricular tachycardia occurred. The intravenous administration of 10 mg Verapamil was followed by total electrical standstill of the heart lasting for more than 24 hours and requiring pacemaker therapy. This case demonstrates that the intravenous administration of Verapamil may be harmful.

Twenty-one patients (3 women, 18 males, mean age 55.7 +/- 6 years) with coronary heart disease proven by coronary angiography entered a double blind randomised study with isosorbide dinitrate slow release 120 mg once a day. 2, 12 and 24 hours after acute medication patients underwent a symptom-limited exercise-ECG. The following parameters were measured: ST-depression, blood pressure, heart rate and working capacity. After one week of therapy the same parameters were measured to look for the development of tolerance. Two and twelve hours after acute medication working capacity increased to 220% and 139% respectively. After 24 hours there was no statistically significant effect. The sum of ST-depression in three leads decreased from 4.85 +/- 3.02 mV to 1.87 +/- 0.96 mV (38.5%; p less than 0.05) 2 hours after medication, and to 2.10 +/- 1.73 mV 12 hours after medication. 24 hours after medication there was still a slight but not significant reduction of ST-depression. There was no statistically significant effect in the placebo group. After one week of therapy there was a slight reduction of action, but no development of tolerance.

Repeated intake of 240-400 mg non-retard verapamil by a 26-year-old male nurse brought about interference dissociation resulting from extreme sinus bradycardia, passive AV nodal rhythm and hypotension. Because of a history of myocarditis a recurrence was suspected and an organic cause of the arrhythmia assumed at first, until its self-inflicted origin was discovered. The case demonstrates the need to consider self-medication, even if at first denied, in the differential diagnosis of arrhythmias even in the absence initially of any clear-cut pointers towards it.

Left ventricular enddiastolic pressure (LVEDP), mean pulmonary artery pressure (PAPM) and enddiastolic pulmonary artery pressure (PADP) were simultaneously recorded in 19 subjects with normal left ventricular (LV) function, and in 109 patients with LV-dysfunction, 83 of whom were also studied during exercise. Patients with valvular heart disease or atrial fibrillation were excluded from this study. LVEDP and mean pulmonary capillary wedge (PCW) pressure were simultaneously recorded in 81 patients at rest, andin 16 patients also during exercise; the LV diastolic pressure prior to atrial contraction (LVPpreA) could accurately be identified in 45 patients at rest and in 23 patients with exercise. In contrast to the widely accepted opinion of others, the PADP (mean 8.2 +/- 2.2 mm Hg at rest and 12.3 +/- 3.4 mm Hg with exercise) showed a close approximation of LVEDP (10.0 +/- mm Hg at rest and 16.2 +/- 3.5 mm Hg with exercise) only in normal subjects at rest (p less than 0.05 and p less than 0.01 respectively). In patients with LV dysfunction there was no significant difference between PADP (11.7 +/- 4.5 mm Hg and 23.0 +/- 8.9 mm Hg), PCW (11.6 +/- 5.1 mm Hg and 24.1 +/- 11.9 mm Hg) and LVPpreA (12.5 +/- 5.5 and 21.5 +/- 7.7 mm Hg) at rest and during exercise. LVEDP could be estimated with sufficient accuracy only from the PAPM (18.9 +/- 6.5 and 35.7 +/- 10.8 mm Hg). The increase in LVEDP (14.7 +/- 7.7 mm Hg) with exercise was not significantly different from the increase in PAPM (16.8 +/- 7.1 mm Hg). There were highly significant correlations (p less than 0.001) between LVEDP and PADP (r = 0.85) as well as PAPM (r = 0.86) at rest and during exercise with the regressionline being closest to the line of identity for LVEDP and PAPM. The pressure gradient between LVEDP and PADP (LVEDP - PADP = 6.3 mm Hg with exercise) equaled the pressure increase in LV by atrial contraction (LVEDP - LVPpreA = 6.3 and 13.3 mm Hg). The pressure difference between PADP or PAPM and LVEDP remained constant despite marked variation of other hemodynamic parameters, e.g. stroke volume index (SVI), heart rate (HR) and cardiac index(CI). These data suggest that an elevated LVEDP is caused mainly by an augmented atrial contraction in patients with LV dysfunction at rest and with exercise. This mechanism precludes an enddiastolic pressure equilibrium between pulmonary artery and left ventricel. PAPM allows the best estimation of LVEDP independent from other hemodynamic variables.

The effect of cigarette smoking on systolic time intervals at rest, with volume overload and with dynamic exercise was studied in nine healthy cigarette smokers. For heart rate, PEP, LVET and blood pressure, reactions to smoking demonstrated considerable interindividual variations with comparable work loads and volume loads. More than half of the subjects developed significant left ventricular dysfunction by these parameters after smoking ten cigarettes. The negative inotropic effect was felt to be caused in these subjects by carbon monoxide. The remaining subjects did not show left ventricular dysfunction with smoking. In these subjects the stimulating effect of nicotine on the nervous system was covering the negative inotropic effect of carboxy hemoglobin.

Electrophysiological effects of the atropin ester Ipatropiumbromide (SCH 1000) were investigated in 15 patients by His electrocardiography and high frequency atrial stimulation. Heart rate increased by 50% of base line heart rate, PA- and AH-intervals and sinus node recovery time decreased, the HF-interval remained unchanged. Physiological av-block by atrial stimulation occurred at significant higher stimulation frequencies with SCH 1000 than without medication. Additional 15 patients were treated for a longer follow-up period. Increase of resting heart rate averaged 15%. Equivocal effects on heart rate were found with exercise after SCH 1000. Non-cardiac side effects were found in 5 patients.