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This case report describes the diagnosis, treatment as well as maternal and fetal outcome of a pregnancy complicated by peripartum cardiomyopathy (PPCM). The article demonstrates criteria that define peripartum cardiomyopathy using clinical and echocardiographic features. In absence of preexisting heart disease an acute left ventricular dysfunction of the mother led to fetal bradycardia and immediate delivery. We discuss possible causes, clinical management and long term outcome in respect of the available literature. Future pregnancies should be avoided with at least 50 % risk of recurrence.

Background and Objective: Implantation of a VDD pacemaker (ventricular pacing; dual sensing [atrial and ventricular]; dual response [triggered + inhibited]) together with a single VDD electrode catheter restores synchronous AV ventricular stimulation in patients with higher-grade AV block and intact sinus function. If higher-frequency stimulation occurs it may be a sign of pacemaker malfunction or of inadequate pacemaker programming. This study was undertaken to determine, at first follow-up examination, in how many patients with a VDD pacemaker VVI stimulation occurred more than 5% of the time; how such patients differed from those with 5% or fewer VVI stimulations; and whether a changed program reduced the proportion of VVI stimulations., Patients and Methods: 67 consecutive patients were tested 1 to 3 months after implantation of the Unity VDD pacemaker (Sulzer Intermedics). The frequency of VVI stimulations was determined via a diagnostic pacemaker memory store. After intermediate analysis, programming was optimized and the patients then re-tested 12 months after the initial implantation., Results: At the first follow-up examination 54 patients had VVI stimulations of < or = 5% (0.5 +/- 0.9%) and 13 had > 5% of the time (19.8 +/- 10.7%). The two groups differed significantly from one another in their lower intervention frequency (< or = 5% VVI stimulations: 47 +/- 6/min; > 5% VVI stimulations: 58 +/- 5/min). In particular, the pacemakers in patients with > 5% VVI stimulations had been significantly more often programmed to values of > 50/min. As a result, the pacemakers of these patients were reprogrammed to a lower frequency. A year after implantation there was no longer any difference in the lower intervention frequency, 44 +/- 4/min, between patients with initially > 5% VVI stimulations and those with initially < or = 5% stimulations. At the same time, the proportion of VVI stimulations fell to 4 +/- 6%, with 67% of patients having AV synchronicity of > 95%., Interpretation: At first follow-up, patients with > 5% VVI stimulations differed from those with < or = 5% stimulations with regard to an increased lower intervention frequency. In most of these patients the proportion of AV stimulations was increased to > 95% by reducing the lower intervention frequency to < or = 50/min.

Although supported by more than 200 years of experience and anecdotal clinical evidence, the efficacy of digitalis in the management of heart failure has been questioned until the past decade. The idea to improve contractility of the diseased myocardium with an inotropic agent is fundamental in the management of left ventricular dysfunction. The majority of clinical trials published since 1980, most of which examined patients with mild to moderate heart failure, indicate that digitalis alone or in combination with vasodilators may improve the clinical outcome particular in those patients with more advanced symptoms and poorer left ventricular function. Aside from its action as an inotropic drug the pharmacology and the mechanisms by which digitalis influence the diseased myocardium and peripheral circulation in heart failure has gained more complexity within the last years, raising the idea of other mechanisms that might be involved in its action. Particular for ACE inhibition multiple clinical trials have conclusively demonstrated its impact on survival and morbidity in congestive heart failure. Improvement of clinical outcome as measured in terms of fewer hospitalizations and improvement of symptoms in patients receiving digitalis seems to be comparable to patients receiving beta-blockers additional to diuretics and ACE inhibitors, an entirely different approach to the treatment of heart failure. Despite initial improvement of hemodynamics it now appears that there is no survival benefit found for digitalis in the management of heart failure.

In this study a correlation was sought between the NYHA class, the results of cardiopulmonary exercise testing (CPX) and the ejection fraction (EF) measured by echocardiography and scintigraphy. Of 36 patients enrolled, CHF in 20 patients was due to CAD and in 16 patients due to DCM. The NYHA class was determined independently by two cardiologists who were blinded to the CPX, echocardiography or scintigraphy results. Sixteen patients were classified as class II and 20 as class III. As a control, 23 patients without cardiopulmonary disease were examined. The CPX was done according to a ramp protocol with continuous measurement of respiratory gases, maximal oxygen consumption (VO2-max) and oxygen consumption at the anaerobic threshold (VO2-AT). A correlation (p = 0.0425) between the NYHA classification and the Weber classification for VO2-AT was found. There was no correlation for VO2-max. VO2-AT was significantly higher in NYHA II patients as compared to NYHA III patients. No significant difference was seen in relation to the VO2-max. In comparison to the normal group, the VO2-AT and VO2-max were significantly lower in NYHA II and III patients. There was no significant correlation between VO2-AT and EF, VO2-max and EF, or between NYHA class and EF. During a 16-month follow-up period lethality was 8/14 patients with VO2-AT < 10 ml/kg/min. Although the NYHA classification provides a valid method for determining the prognosis of CHF patients, if feasible, the CPX examinations should be used to provide updates of the disease progress.

The purpose of this study was to assess cardiopulmonary exercise capacity, variation in heart rate during everyday activities, frequency of atrial arrhythmias and quality-of-life during accelerometer-based rate modulated dual-chamber pacing. Nine chronotropically incompetent and 14 chronotropically competent patients (mean age 51 years) were randomly assigned to DDD and DDDR mode and evaluated by a semisupine bicycle exercise testing exceeding the anaerobic threshold, 24-h Holter monitoring and a quality-of-life questionnaire. In the subgroup of patients with chronotropic incompetence, defined by a HR/VO2-ration, 2 beats/ml/kg, during DDDR pacing, compared to DDD, maximum heart rate increased from 83 +/- 13 to 132 +/- 7 beats/min (p < 0.01), maximum oxygen uptake from 12.7 +/- 3.1 to 15.3 +/- 3.2 ml/kg/min ( p < 0.05) and the VO2/WR-ratio from 8.1 +/- 1.0 to 9.0 +/- 0.9 ml/min/watts (p < 0.05). Exercise duration lengthened from 252 +/- 59 to 301 +/- 96 s (p < 0.05). During the 24-h Holter recordings the average maximum heart rate rose form 69 +/- 7 in the DDD mode to 78 +/- 9 beats/min in the DDDR mode significantly (p < 0.05). DDDR pacing did not result in an increased number of atrial salvos (2.6 atrial events/24 h) when compared to DDD pacing (2.5 atrial events/24 h, N.S.). These objective results were confirmed by the quality-of life assessment due to a symptom questionnaire. The symptom score declined from 20 +/- 10 in the DDD mode to 16 +/- 7 in the DDDR mode (p < 0.01). In the patients with chronotropic competence, however, cardiopulmonary exercise capacity did not improve in the DDDR mode: maximum heart rate was 120 +/- 21 versus 130 +/- 24 beats/min (N.S.), maximum oxygen uptake 17.7 +/- 5.9 versus 16.8 +/- 5.9 ml/kg/min (N.S.), The VO2/WR-ratio 9.8 +/- 2.3 versus 9.2 +/- 2.5 ml/min/watts (N.S.) and the exercise duration 407 +/- 159 versus 406 +/- 165 s (N.S.). The average maximum heart rate was 80 +/- 15 in the DDD mode and 83 +/- 16 beats/min in the DDDR mode (N.S.). Significantly more atrial arrhythmias occurred in the DDDR pacing mode: 1.6 atrial salvos per 24 h in the DDD mode versus 4.8 atrial salvos per 24 h in the DDDR mode (p < 0.05). This patient subgroup experienced a significant worsening of his quality-of-life. The symptom score rose from 20 +/- 9 in the DDD mode to 28 +/- 11 in the DDDR mode (p < 0.05). In conclusion, DDDR pacing improved cardiopulmonary exercise capacity, normalized heart rate variation over 24 h and increased quality-of-life in patients with chronotropic incompetence. On the contrary, since the DDDR pacing more could not improve cardiopulmonary exercise capacity, increased atrial arrhythmias and worsened the patient's quality-of-life, patients with chronotropic competence should not be programmed in the DDDR pacing mode.

Cardiovascular manifestations are a frequent finding in hypothyroidism. Thus, blood-pressure measurements, longtime electrographic monitoring, and spiroergometry were examined in 20 patients with transitory hypothyroidism. In the patients with thyroid carcinoma, total thyroidectomy was performed. Measurements were made in hypothyroidism and after TSH-suppression with L-thyroxine. Thirty-five patients in whom intracardiac catheter examination ruled out cardiopulmonary disease served as controls. Cardiopulmonary exercise was done by bicycle exercise testing. In transitory hypothyroidism an increase of diastolic blood pressure was found at rest (p = 0.02) and during exercise (p = 0.002), which was reversible after T4-therapy. Compared to the controls diastolic blood pressure in hypothyroidism was increased at rest (p = 0.014) and during exercise (p = 0.005). ECG-monitoring showed a day-night difference in heart rate in hypothyroid patients and after therapy. The mean heart rate (74 vs. 88 beats per minute; p = 0.0006), the minimal (p = 0.0062) and the maximal heart rate (p = 0.0016) during the day were decreased in hypothyroidism compared to euthyroidism. There were no atrioventricular blocks in transitory hypothyroidism and no increase of ventricular or supraventricular premature beats after high-dose T4-treatment. Spiroergometry showed no change in ventilation and an increased growth in heart rate (p = 0.021) associated with good working capacity in hypothyroid patients. Heart rate at rest (p = 0.004) and at the anaerobic threshold (p = 0.03) were decreased in transitory hypothyroidism.

VDD stimulation is an alternative to DDD pacing due to the possibility of p-wave synchronous ventricular pacing without the need of an atrial lead. Mainly, the reliability of the system depends on the atrial sensing. In 22 patients the intraoperative atrial amplitude and, postoperatively, the atrial sensing threshold were measured. Furthermore, the stability of the atrial sensing threshold during follow-up was proven. The mean atrial amplitude was intraoperative by 2.4 +/- 1.2 (1.0-6.8) mV. The measurement of the atrial sensing threshold in the first 5 postoperative days showed a mean value of 1.02 +/- 0.49 (0.3-1.6) mV. The measurements of the mean atrial sensing threshold after 30, 90, and 180 days showed no statistical differences. Intraindividual variance was shown in 17/20 patients (0.55 +/- 0,42; 0.15-1.05 mV). Seventeen of the 22 patients were programmed with an atrial sensing threshold of 0.3 mV. In five patients the atrial sensing threshold was programmed at less than 0.3 mV in order to reach a twofold atrial sensitivity. Despite a programmed atrial sensitivity of 0.1 mV and isometric conditions no atrial oversensing occurred. The postoperative atrial sensing thresholds of the VDD system investigated were significantly lower than the intraoperatively measured atrial amplitudes. The mean atrial sensing threshold did not change during the follow-up period. The variation which did occur was within individual variation at different return visits.

The prevalence of myocardial bridging in patients with angina pectoris but normal coronary arteries was evaluated in 1780 patients who consecutively underwent coronary angiography. 62 patients (3.5%) were free of coronary atherosclerosis or other organic heart disease. In four of these patients systolic narrowing of the LAD was present. The other 58 patients received 0.2 mg nitroglycerin (NTG) intracoronarily and 30 micrograms/ml orciprenalin (ORC) intravenously up to a heart rate of 130/min. Repeated angiography revealed systolic compression of the LAD due to myocardial bridging (MB) in 40% (25 of 62). The length of MB raised from 1.4 +/- 0.9 cm to 2.1 +/- 1.1 cm (p < 0.001) after NTG and to 2.8 +/- 1.1 cm (p < 0.001) after ORC. Coronary luminal stenosis increased from 48 +/- 29% to 67 +/- 25% after NTG (p < 0.001) and to 83 +/- 18% (p < 0.001) after ORC. The prevalence of myocardial bridging in 40% of patients with stress-induced angina pectoris but normal coronary arteries is high. Nearly always coronary compression by myocardial bridging is only evident after adrenergic stimulation or after afterload reduction. Therefore, NTG and ORC are useful drugs to facilitate diagnosis of myocardial bridging by increasing coronary compression.

Patients: Three patients complained of proximal weakness and paraesthesia of the legs and difficulties in walking during amiodarone treatment. Examination showed signs of a predominantly distal sensory neuropathy, a proximal myopathy, and a cerebellar gait disorder. All had amiodarone dosages of 600 mg per day, amiodarone serum levels above 2.7 mg/l and a total amount of amiodarone ingestion of 300 to 500 g. The clinical symptoms subsided within six to eleven months after treatment was stopped., Results: The neurophysiologic investigations showed slowing of sensory and motor nerve conduction velocities with dissociation of the action potentials and delay of SEP latencies. With discontinuation of the drug these abnormalities were progressive in one patient. The biopsy (muscle, nerve and skin) in the most severely affected patient showed numerous intracellular lysosomal inclusions in cells of different tissues. It is supposed that the storage of amiodarone in muscle cells results in a predominantly proximal myopathy whereas storage in Schwann cells results in a secondary neuropathy. A similar storage in Purkinje cells may be responsible for the cerebellar gait disorder., Conclusion: The clinical picture should be termed a neurotoxic amiodarone syndrome rather than amiodarone neuropathy.

This study was designed to assess the effect of acute minute ventilation sensing, rate-responsive pacing on cardiopulmonary exercise capacity in 27 patients (mean age 60 years) with chronotropic incompetence. The exercise protocol consisted of bicycle exercise in semisupine position with breath-to-breath analysis of gas exchange. At the anaerobic threshold heart rate increased from 75 +/- 9 in the VVI-mode to 113 +/- 21 beats/min in the VVI-R-mode (p < 0.001), oxygen uptake from 9.3 +/- 3.4 to 10.9 +/- 4.3 ml/kg/min (p < 0.001) and work rate from 52 +/- 20 to 65 +/- 24 watts (p < 0.001). Compared to 41 normal subjects, VVI-R pacing increased oxygen uptake up to 75% and work rate up to 79% of normal values, while heart rate increased similarly in both groups. The VO2 to work rate ratio (dVO2/dWR), calculated as the slope of the relation of oxygen uptake to work rate below the anaerobic threshold, improved from 7.9 +/- 2.3 to 10.2 +/- 2.4 ml/min/watts (p < 0.001) in the VVI-R-mode; so it did not differ from normal values. Thus, acute respiratory dependent rate-responsive pacing results in substantial improvement in cardiopulmonary exercise capacity in patients with chronotropic incompetence. The VO2 to work rate ratio demonstrated to be a reliable parameter for assessing this improvement.

Normal values for cardiopulmonary bicycle exercise testing in semisupine position using a ramping protocol in a middle-aged group of untrained men and women are presented. We exercised 23 men and 16 women aged from 33 to 66 years without evidence of cardiopulmonary or cardiovascular disease and normal findings during complete heart catheterization. Clinical findings, x-ray, resting and exercise ECG, and laboratory findings were normal. Exercise testing was performed using a ramping protocol with a work rate increase of 20 watts/min. Respiratory gas analysis (breath-to-breath method) was performed and oxygen uptake (VO2), carbon-dioxide production (VCO2), and minute ventilation (VE) were determined at maximal work load and at the ventilatory anaerobic threshold. Work rate increase and heart rate were continuously monitored. From these data oxygen pulse, the respiratory quotient (RQ), and the ventilatory equivalents VE/VO2 and VE/VCO2 were derived. Furthermore, the VO2 to work rate ratio, and the VO2 to heart rate ratio were analyzed. Maximal VO2 was within the 95% confidence interval of predicted VO2max. The anaerobic threshold (V-slope method) was 60% of VO2 max at the RQ of 0.81 for men and 66% of VO2max at the RQ of 0.84 for women. The O2 pulse was 100% of the age predicted value. The VO2 to work rate ratio was 10.7 +/- 1.4 for men and 9.7 +/- 1.2 ml/watts/min for women (p < 0.05). The slope of heart rate to VO2 from rest to peak exercise as a measure of chronotropic competence was nonlinear in 59% of the subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

A large asymptomatic aneurysm of the internal carotid artery containing a free floating thrombus was detected in a 90-year-old woman. The alteration was documented by duplex sonography of the extracranial carotid arteries. At a second examination 4 days later the thrombus was observed to be fixed to the dorsal and distal aneurysm wall. With regard to the age and reduced general state of health of the patient, invasive diagnostic examinations and reconstructive surgery were not indicated and the patient was released in a good condition.

Spiroergometry might be applicable to detect alterations of cardiopulmonary functions related to hyperthyroidism. Thus, cardiac and respiratory changes as well as work capacity in hyperthroid female patients were to be assessed with the help of the Cardiopulmonal Exercise Test System. Twelve female hyperthyroid patients with Graves' disease of whom all were controlled in euthyroidism, were examined. Eighteen euthyroid female patients in whom intracardiac catheter examination ruled out cardiopulmonary disease served as controls. The anaerobic threshold was determined by means of the V-slope method. An echocardiography was performed in all patients. Ergometry was performed in a semisupine position using a continuous ramp protocol of 20 watt/min. A markedly reduced work capacity, and a high heart rate in rest and exercise were found. In the ratio heart rate/oxygen uptake a lower rise (p = 0.001) due to a decreased growth in the heart rate was noticed. Regarding the pulmonary system a decreased tidal volume in hyperthyroidism (p = 0.021), and a higher breathing frequency (p = 0.003) were recognized, as well as an impaired oxygen consumption, in comparison with the euthyroid state. Also, echocardiographically an increased cardiac index (p = 0.008) and a markedly reduced stroke volume (p = 0.005) in comparison to the control group were observed. Heart rate, work capacity, oxygen uptake, and the ratio heart rate to oxygen uptake were normalized in euthyroidism. With the help of the CPX-System noninvasive measure of marked cardiopulmonary changes in hyperthyroidism are possible, especially the lower growth of the heart rate in exercise, which might be the limiting factor of work capacity.

Incidence and type of cardiac complications in 701 patients undergoing arterial vascular surgery were prospectively investigated to identify high-risk groups. Cardiac morbidity was 10.1%. Cardiac complications were responsible for 28 deaths (57%). Using logistic regression analysis, age (cardiac morbidity greater than 7017.3%), impaired renal function (19.8%), and congestive heart failure (17.3%) were the main independent risk factors. In addition, 4 risk factors (arrhythmia, coronary artery disease, anemia, emergency surgery) showed significant individual association with cardiac complications. Cardiac morbidity increased to 27.8% in patients with more than 2 of these 7 risk factors. A further association could be demonstrated between the degree of peripheral vascular disease and cardiac morbidity, but not with the extent of the operation. Based on our results a distinction between three groups of different cardiac risk can be made. A clinical algorithm for further cardiac assessment in high-risk patients is presented.

From March 1983 to June 1986 in 206 patients with acute transmural myocardial infarction, combined intravenous and intracoronary therapy with streptokinase was initiated. After intravenous thrombolysis and randomization in two groups we performed a coronary angiography with selective intracoronary lysis. Infarct related vessels still occluded after intracoronary streptokinase application were opened mechanically in group I. In group II we performed additionally a percutaneous transluminal coronary angioplasty (PTCA) after mechanical recanalisation (occluded vessels) or after thrombolysis (open vessels). In 85 of 87 cases in group II, PTCA could be performed in the acute phase. Elective PTCA was performed in 22 patients of group I (21%) and in nine patients of group II (9%). Up to five years after myocardial infarction, coronary artery bypass grafting (CABG) was necessary in 22 patients (21%) of group I and in 23 patients (22%) of group II. Within four weeks after infarction CABG was performed in 32% and 17% of group I and II respectively. The six-year survival rate was 78% in group I and 82% in group II. Taken all patients together, the six-year survival rate was significantly higher (p = 0.002) for those with early reperfusion (less than or equal to 3.5 h). The survival rates of CABG-patients, PTCA-patients and patients without reperfusion were 91%, 74% and 65% respectively. Streptokinase thrombolysis results, combined with acute or elective PTCA and/or coronary bypass surgery, in a high six-year survival rate after acute transmural myocardial infarction. This rate is about 20% higher than ten years ago.

The influence of the AV interval on early passive (E) and late active diastolic filling (A) during transmitral flow was analyzed in patients with AV sequential pacing. In 16 patients with dual-chamber pacemakers at the age of 25 to 76 years CW- and color Doppler echocardiography was used to determine inflow time (t), flow velocity (Vmax), the E/A ratio, the time-velocity integral (TVI), and the inflow jet at constant AV sequential pacing (80 bpm) with various AV interval settings (50-100-150-200-250 ms). The inflow pattern was compared to findings in 16 normals (age 26 +/- 7 years). The prolongation of the AV interval from 50 to 250 ms resulted in the following changes: 1) Decrease of tE: 220 +/- 30 ms to 170 +/- 40 ms (p less than 0.05), of VmaxE: 78 +/- 12 to 68 +/- 14 cm/s) (ns) and of TVI-E: 8.5 +/- 2.1 to 5.6 +/- 1.7 cm (p less than 0.001); 2) Increase of tA: 140 +/- 30 to 270 +/- 60 ms (p less than 0.001), of VmaxA: 48 +/- 18 to 73 +/- 24 cm/s (p less than 0.001) and of TVI-A: 2.4 +/- 1.1 to 6.1 +/- 2.9 cm (p less than 0.001); 3) Decrease of the E/A ratio from 1.6 +/- 05 to 0.85 +/- 02. Longer AV intervals shortened the total diastolic filling period and produced more diastolic aliasing without change of the relative diastolic inflow jet. The AV interval of 150 ms was associated with an abnormal high atrial component of transmitral inflow, as found with abnormal diastolic LV function.(ABSTRACT TRUNCATED AT 250 WORDS)

Incidence and clinical significance of cardiac side effects of extracorporeal shock-wave lithotripsy (ESWL) were prospectively analysed for 85 patients (26 men, 59 women; mean age 44 [17-81] years) with cholecystolithiasis (n = 70) or choledocholithiasis (n = 15). 24-hour ECG monitoring was undertaken on the day of treatment. Additionally, during ESWL cardiac rhythm and blood pressure were monitored. ESWL was performed with an electromagnetic lithotriptor under light anaesthesia with intravenous diazepam (10 mg) and pethidine (75-100 mg). There were no superventricular premature systoles in any of the patients during treatment. In 15 patients with occasional ventricular premature systoles (VPS) (6-81 per 23 hours) in the 24-hour ECG the number of VPS increased during the one-hour ESWL procedure significantly to 6-55 (P less than 0.05). 14 of these patients had an unremarkable cardiac history. Changing the lithotriptor coupling angle failed to suppress the VPS in only two patients. In these two it was necessary to trigger the shock wave with the ECG. Blood pressure rose markedly (up to 220 mm Hg systolic) during ESWL in only three patients, known hypertensives. But this rise was easily controlled with nifedipine, 10 mg sublingually. These data demonstrate that ESWL is a safe alternative to operative treatment, even in the presence of existing cardiac disease. Nonetheless, precautions should be taken in case there are complications.

In patients with coronary heart disease platelet activity may be pathologically increased. Administration of platelet inhibitor drugs is an established treatment principle. The interactions between platelet activation, platelet inhibitor drugs like acetylsalicylic acid (ASA) or molsidomine and the endogenous fibrinolysis were studied in three trials. Platelet aggregation and thromboxane synthesis are dose- dependently inhibited after oral intake of ASA (0, 10, 30, 100 or 500 mg/d) Additional intake of the antianginal agent and nitric oxide donator Molsidomine (8 mg) results in a synergistic platelet inhibitor effect characterized by a significantly delayed aggregation response. In a group of patients with coronary artery stenoses platelet activity was markedly enhanced, when compared to healthy individuals. During physical exercise platelet activity was even further enhanced and plasma t-PA-activity was increased by a factor of 2.2. The stimulation of the endogenous fibrinolytic system was markedly reduced when compared to healthy subjects. Following successful coronary angioplasty 393 patients were randomized to receive either molsidomine (2 x 8 mg/d) or ASA (1 x 500 mg/d) plus nifedipine (3 x 20 mg/d). Coronary angiography performed after the 6 month treatment period revealed a restenosis rate of 29% in the molsidomine group and of 33% in patients treated with ASA + nifedipine. This difference was not statistically significant.

Potentially malignant ventricular arrhythmias are common in chronic heart failure. The aggravation of such arrhythmias has many causes in these patients and cannot be predicted. Therefore, proarrhythmia due to PDE-inhibitors which increase cytosolic calcium levels by specific inhibition of the degradation of cyclo-AMP may be difficult to recognize. A retrospective analysis of 24-h Holter ECG was performed in 31 patients (NYHA classes III and IV) under long-term enoximone therapy. At baseline, 68% of the patients had ventricular couplets and nonsustained ventricular tachycardia. After a mean treatment period of 7 months, 10% of the patients showed a significant increase, 16% a significant decrease (greater than 90%) of ventricular couplets and salvos, and an additional 32% of the patients showed a significant decrease (greater than 70%) of single PVCs. The change of the arrhythmia profile was not related to the clinical course in these patients. Furthermore, 24-h Holter recordings were analyzed in a randomized long-term trial with captopril and enoximone that included 20 patients of NYHA class II. Despite comparable baseline findings, a reduction of cardiopulmonary exercise capacity was observed in patients treated with enoximone, but not with captopril. However, the arrhythmia profile was similar in both treatment groups. These findings suggest that, in most patients with advanced chronic heart failure, long-term enoximone therapy is not associated with an important increase of ventricular arrhythmias. According to the 24-h Holter findings of the European Enoximone Data Bank, proarrhythmia can be expected in 12% of all patients. Control of the arrhythmia profile, however, is mandatory, because the incidence of proarrhythmia cannot be predicted in the individual patient.

Based on the linear relationship between cardiac output and oxygen uptake direct breath-to-breath gas exchange measurements during exercise allow accurate determinations of cardiopulmonary function. We used cardiopulmonary exercise testing to assess the physiologic benefit of rate response VVIR pacing in 17 patients with chronotropic incompetence. 13 patients had an activity-rate-response pacemaker, two patients had a temperature-controlled pacemaker and two patients a respiratory-dependent system. Exercise testing was performed with the pacemaker, either programmed to fixed rate VVI or to rate variable VVIR pacing. All patients were exercised on a bicycle using a ramp protocol with 10 to 20 watts/min increments. Maximal oxygen uptake and the anaerobic threshold were determined. Compared with findings in the VVI mode, rate response VVIR pacing increased maximal exercise heart rate from 74 +/- 10 to 118 +/- 21 bpm (p less than 0.001). This increase in heart rate was associated with an increase of maximal oxygen uptake from 14.3 +/- 5 to 18.3 +/- 6 ml/kg per min (p less than 0.04) and a delay of the anaerobic threshold to a higher oxygen consumption of 14.6 +/- 5 vs 10.6 +/- 5 ml/kg per min (p less than 0.04). The individual increase in oxygen uptake was a direct function of the change in exercise heart rate independent of the implanted pacing device. The improved aerobic capacity resulted in a 17% increase in exercise tolerance and a 19% increase of exercise time. Cardiopulmonary exercise testing appears to be a useful noninvasive technique to quantify the cardiopulmonary benefit of rate response pacing.

Cardiac frequency could not be lowered in a 62-year-old patient with atrial flutter and 2:1 conduction. Using an electrode catheter positioned in the His bundle area an electric current of 80 Ws was effected. A third-degree atrioventricular block developed which regressed after 6 hours. The electrophysiologic assessment after one week showed a marked diminution of AV node conduction capacity.

One- and two-dimensional echocardiographic findings in 17 patients with dilated cardiomyopathy were compared with haemodynamic and angiographic results of cardiac catheterization. In a further 52 unselected patients with dilated cardiomyopathy, who had been seen as out- or in-patients over a period of two years, the frequency of intracardiac thrombi was investigated echocardiographically. A significant correlation (r = 0.66 and r = 0.68) was found between echocardiographically determined left-ventricular end-diastolic and end-systolic volumes on the one hand and volumes determined angiographically on the other. However, ventricular volumes were clearly underestimated by echocardiography. In contrast, both methods showed good agreement for the magnitude of the ejection fraction (r = 0.79). The aortic valve opening surface estimated with one-dimensional echocardiography correlated with left-ventricular ejection volume (r = 0.93). Thrombi were demonstrated in 7 out of 52 patients: 5 were located in the left, one in the right and a further one in the central pulmonary vascular system. Considering the aforementioned limitations, echocardiography is a useful method for evaluation of left-ventricular function and for demonstration of intracardiac thrombi in dilated cardiomyopathy.

The effect of beta-adrenergic receptor stimulation on sinus node function in patients with sick-sinus syndrome was investigated. Electrophysiological studies were performed in 14 patients (5 males and 9 females) aged 18-81 years before and after intravenous administration of 50 micrograms Prenalterol per kilogram body wt. Prenalterol decreased spontaneous cycle length by 26% (p less than 0.01), which corresponded to an increase in heart rate of 21 beats/min. The corrected sinus node recovery time was shortened by 23% (n.s.) in 10 patients, and was abnormal in 12 patients before and in 10 patients after Prenalterol. Secondary pauses occurred in 8 patients at control and in 9 patients after drug administration, in 2 of them for the first time after Prenalterol. In the sick-sinus syndrome the pronounced chronotropic response to beta-adrenergic receptor stimulation with Prenalterol doses not indicate improvement of impaired sinus node function.

Of 350 patients who had extensive non-invasive and invasive cardiological diagnostic tests, 56 had completely normal results. 24-hour ECG monitoring of the latter revealed the following ventricular arrhythmias-ventricular extrasystoles (VES): 36% without, 23% with rare ones (less than 30/h), 5.4% with more than 30/h, 25% with polytopic VES, 7.1% with paired VES and 3.6% with ventricular tachycardia. There was no preferential VES pattern. Mean duration of VES was 0.15 s. There were no VES with a prematurity index of less than 1. Extending ECG monitoring to 96 hours (10 persons without heart disease) did not reveal any more significant VES, but registering for less than 24 hours definitely underestimated the frequency of VES in persons without heart disease. In those without angiographic evidence of heart disease 36% had complex and 5.4% frequent VES. Complex arrhythmias, however, are rare in the individual subject and generally not accompanied by frequent VES. Frequent complex arrhythmias or both frequent and complex arrhythmias, as well as VES with a prematurity index less than 1, are suggestive of organic heart disease.

The diagnosis of dilated (congestive) cardiomyopathy was made in 75 patients on the basis of clinical, ECG, echo and angiographic-haemodynamic findings. Ambulatory 24-hour monitoring was undertaken in all patients. Nearly all of them (93%) had ventricular extrasystoles (VES), 35% more often than 1000/24 h. In 15% VES occurred in pairs, in 44% as ventricular tachycardia. In general, frequent VES (greater than 30/h) also came in pairs and/or as ventricular tachycardia. On the other hand, not all patients with such complex arrhythmias also had frequent VES. In about 70% of all patients with ventricular tachycardia such episodes were registered repeatedly, in more than 40% more than five tachycardia episodes per 24 hours. In the majority of patients the tachycardia consisted of three (33%), four (12%) or five (18%) consecutive ventricular complexes. All episodes of ventricular tachycardia ended spontaneously and were clinically largely silent. Apparently there was no clinically relevant correlation between frequency and severity of the arrhythmia, on the one hand, and extent of abnormal ventricular function, on the other. These findings indicate that frequent and complex ventricular arrhythmias are a characteristic feature of dilated (congestive) cardiomyopathy. If they occur in heart disease of seemingly unknown aetiology, dilated cardiomyopathy should be suspected. Preliminary findings of long-term observation indicate that patients with frequent ventricular tachycardias have a higher risk of sudden death.

A separation of the left atrium from the right pulmonary artery during atrial contraction may be observed in the suprasternal echocardiogram. In 280 catheterized patients with sinus rhythm, we investigated whether left atrial separation is a parameter from which an estimate of the left atrial pressure can be obtained. In 239 of the 280 patients, the suprasternal echograms were of a quality such that it could be seen whether there was, a left atrial separation. In 182 patients, a normal left atrial pressure (greater than or equal to 12 mm Hg) was found; in 57 patients, the left atrial pressure was elevated. An atrial separation was observed in 183 patients, and in 56 patients it was lacking. Lack of left atrial separation indicates a left atrial pressure elevation with a sensitivity of 73.7% and a specificity of 92.3%. If a left atrial pressure above 18 mm Hg was considered elevated, the sensitivity of this echoparameter amounted to 90.3%, and the specificity was 86.5%. The study shows that the left atrial separation from the right pulmonary artery separation from the right pulmonary artery in the suprasternal echocardiogram is a parameter valuable in providing a rough estimate of the left atrial pressure.

The incidence and severity of ventricular arrhythmias was analyzed in 42 patients with pure or predominant mitral valve stenosis (age: 51 +/- 9 years; NYHA class: 2.7 +/- 0.5) and 23 patients with pure or predominant mitral valve regurgitation (age: 55 +/- 11 years; NYHA class: 2.7 +/- 0.6) employing 24 h ambulatory monitoring. Coronary artery disease was excluded by angiography in all patients. Ten patients (14%) had no ventricular premature beats (VPB), 5 patients (7%) greater than 1,000 VPB/24 h, 31 patients (44%) multiform VPB, 19 patients (27%) repetitive VPB and 7 patients (10%) ventricular tachycardia. There was no difference in VPB between patients with mitral valve stenosis and mitral valve regurgitation. The incidence and severity of ventricular arrhythmias was significantly higher (p less than 0.001) in patients with mitral valve disease compared to the VPB of 50 normals without identifiable heart disease. This was still valid, if only patients with normal left ventricular ejection fraction greater than 55% (n = 60) were compared (p less than 0.01). The occurrence of frequent and complex ventricular arrhythmias was not determined by age, NYHA class, pulmonary artery pressure, pulmonary artery resistance, size of the left atrium, mitral valve area, degree of mitral regurgitation or cardiac index. However, a significant inverse correlation was found between incidence and severity of VPB and left ventricular ejection fraction. A reduced right ventricular ejection fraction, on the other hand, barely affected the occurrence of complex ventricular arrhythmias. Thus frequent and complex ventricular arrhythmias may be a sign of reduced left ventricular function in patients with mitral valve disease.

The study was performed to evaluate the combined effect of thrombolysis therapy and percutaneous coronary transluminal angioplasty (PTCA) on global and regional left ventricular function. In 127 patients with acute transmural myocardial infarction combined intravenous (250 000 U) and intracoronary (50 000 U) streptokinase therapy was started. When the infarct related vessel was occluded mechanical recanalization was performed with recanalization by Gruentzig balloon catheters. Patients were randomized in two groups, group I, n = 64, thrombolysis without PTCA; group II, n = 63, thrombolysis with PTCA. Both groups demonstrated no difference in relation to sex, age, infarct location, as well as CPK levels and time between onset of symptoms and start of treatment. First coronary angiography showed an open vessel in 23/64 patients (36%) of group I and in 12/63 patients (19%) of group II (p less than 0.001). Mechanical recanalization with 3 F catheters could be achieved in 27/41 patients (66%) of group I and with 4 F catheters in 26/51 patients (51%) of group II. In 9/41 patients (22%) of group I and in 18/51 patients (35%) in group II reperfusion took place before mechanical recanalization could be performed or occurred during superselective thrombolysis therapy, when mechanical recanalization failed. Thus, reperfusion rate in group I was 59/64 patients (92%) and in group II 56/63 patients (89%). PTCA was attempted in 55/56 patients in group II with a success rate of 65% and reocclusion rate of 4%. During hospital stay, reocclusion occurred in 10/59 patients in group I (17%) and in group II in 9/55 patients (16%). The patients were divided in those with and without successful angioplasty. Reocclusion was found in 3/36 patients (8%) and 6/17 patients (35%), respectively. Improvement with PTCA of regional and global left ventricular function was observed in patients with anterior myocardial infarction. With combined medical-mechanical recanalization, reperfusion rate can be increased and infarct time shortened, thus, providing the possibility of full revascularization by PTCA, improving coronary blood flow as well as improving global and regional left ventricular function.

The arrhythmogenic potential of long-term treatment with Enoximone in patients with severe chronic heart failure has not been determined. We analysed retrospectively 24 h Holter recordings in 31 patients with chronic heart failure, predominantly NYHA functional class III and IV, before and during chronic Enoximone therapy between 4 and 52 weeks. At baseline ventricular couplets and salvos were found in 68% of patients. Ventricular arrhythmia response was variable with no significant overall change. During a mean follow-up of 28 weeks, however, 3 (10%) patients showed a significant increase and 4 (16%) patients a more than 90% decrease of repetitive ventricular arrhythmias. In another 10 (32%) patients a more than 70% decrease of singular ventricular arrhythmias was observed. There was no correlation between the change of the patient's arrhythmia profile, the degree of functional impairment of the underlying heart disease, and the clinical response to long-term Enoximone therapy. Two patients died suddenly, one with a significant increase, the other with a significant reduction of ventricular arrhythmias. Two patients died of pump failure with no change of the arrhythmia profile. Enoximone appears to have a low arrhythmogenic profile during long-term treatment. However, careful monitoring of ventricular arrhythmias is mandatory as the occurrence of proarrhythmic drug effects cannot be predicted.

Effect and tolerance of the oral phosphodiesterase inhibitor Enoximone was tested in 14 patients with advanced cardiac failure (New York Heart Association groups II-IV). During a mean observation period of 40 weeks there were four deaths; one patient became therapy-resistant. The remainder reported sustained clinical improvement. During the observation period there were no changes in heart rate or arterial blood pressure. There were no significant changes in cardiothoracic ratio on the chest X-ray or of the echocardiographically determined left-ventricular diameters. However, there was a rise in shortening fraction from 13.5 +/- 6.4% to 16.8 +/- 6.5% after 26 weeks, and to 21.1 +/- 8.1 after 52 weeks (P less than 0.05). The ratio of the systolic time intervals, PEP/LVET, decreased correspondingly from 0.74 +/- 0.23 to 0.44 +/- 0.09 and 0.43 +/- 0.10 (P less than 0.05). Hemodynamic measurements after one-year treatment revealed an increase in cardiac index from 2.4 +/- 0.7 to 3.6 +/- 0.6 l/min X m2, and a fall in pulmonary artery wedge pressure from 25.5 +/- 9.7 to 12.6 +/- 13.0 mm Hg (P less than 0.001). The drug was well tolerated and there were no significant biochemical changes. Long-term ECG monitoring revealed no significant changes in the arrhythmia profiles. Enoximone thus proved to be a successful therapeutic agent in the management of advanced heart failure.

Unlabelled: In 200 consecutive patients with acute myocardial infarction combined medical-mechanical recanalization was attempted. Coronary angiography revealed an occluded vessel in 150 patients. This vessel could be opened in 127 patients. There were 112 men and 15 women, aged 32 to 72 years (mean age 61.2 years); 60 patients had an anterior and 67 patients presented with an inferior myocardial infarction. 103 from 127 patients presented with arrhythmias during the ischemic phase and 112 from 127 patients during the reperfusion phase. The following arrhythmias had a significantly higher incidence in the reperfusion phase compared to the ischemic phase: sinus bradycardia (29 pts. - 22.8% - vs. 15 pts. - 11.8%; p less than 0.05), ventricular bigeminy (28 pts. - 29.9% - vs. 5 pts. - 3.9%; p less than 0.01), ventricular couplets (34 pts. - 26.8% - vs. 20 pts. - 15.7%; p less than 0.05) and accelerated idioventricular rhythm (32 pts. - 25.2% - vs. 5 pts. - 3.9%; p less than 0.01). Ventricular fibrillation occurred during the ischemic phase in 9 patients and during the reperfusion phase in 7 patients (n.s.). None of the patients presented with sustained ventricular tachycardia, neither in the ischemic, nor in the reperfusion phase., Conclusions: The following rhythm disturbances can be called reperfusion arrhythmias: sinus bradycardia, ventricular bigeminy, ventricular couplets and accelerated idioventricular rhythm. The observed reperfusion arrhythmias were short-living and did not need special therapeutic measures.

The influence of the autonomic nervous system on sinus node automatism was assessed in 61 patients with suspect sinus node dysfunction. Cardiac frequency and corrected sinus node recovery time (CSNRT) were determined before and after functional autonomic blockade with intravenously administered propranolol (0,2 mg/kg) and atropine (0,04 mg/kg). A pathologic CSNRT was found in 59% of patients before and in 54% after autonomic blockade. In 44% pathologic CSNRT occurred during both conditions. In these patients intrinsic sinus node disease can be assumed. In 15% of patients an initially pathologic CSNRT became normal after blockade. In these patients sinus node dysfunction is caused by autonomic dysregulation. In 10% of patients pathologic CSNRT was seen for the first time after blockade. In such patients an altered autonomic balance seems to camouflage the primary intrinsic sinus node disease. Abnormal intrinsic cardiac frequency (cardiac frequency after autonomic blockade) was observed in pathologic prolongation of CSNRT after blockade, however not in normal CSNRT. On the other hand only 39% of patients with prolonged CSNRT after blockade had at the same time an abnormal intrinsic cardiac frequency. Autonomic blockade improves the diagnosis of the sick sinus node syndrome. Demonstration of abnormal intrinsic cardiac frequency is highly specific of intrinsic sinus node disease. Normal intrinsic cardiac frequency does, however, not exclude intrinsic sinus node disease.