Beta-blockers for heart failure: is slowing of heart rate essential?
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Biomedical subjects
Publications and source records attributed to M Tendera.
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UNLABELLED: Respiratory rate is an important factor influencing heart rate variability (HRV), but is usually ignored in the studies in patients with ischaemic heart disease (IHD). This factor may significantly contribute to the changes in HRV in ischaemic left ventricular impairment. We examined 186 patients with IHD (46 females, 140 males), including 54 pts with left ventricular ejection fraction < 40% and 132 pts with preserved LVEF (> or = 40%). HRV was evaluated in supine and standing position from short-term ECG (512 beats, 1 kHz, 12 bit) in time- (mean RR interval--RRI, and standard deviation of RRI-SD-RR) and frequency-domain (FFT). Power spectral density of high and low frequency (HF 0.14-0.5 and LF 0.04-0.15 Hz) was estimated and expressed as log-values. The frequency of respiration (fResp, Hz) was defined as the frequency of maximum HF power. RESULTS: Patients with LVEF < 40% had shorter RRI in supine (879 + 157 vs 942 +/- 147 ms, p < 0.05), but similar in standing. FResp was greater both in supine (0.308 +/- 0.05 vs 0.274 +/- 0.047 Hz) and in standing (0.329 +/- 0.055 vs 0.274 +/- 0.047, all p < 0.001) in low, as compared to preserved LVEF. As expected, HRV parameters were more reduced in LVEF < 40%. The differences of raw values were as follows: SD-RR 29 +/- 16 vs 34 +/- 15 i 27 +/- 13 vs 31 +/- 12 ms, both p < 0.05, HF 3.21 +/- 0.36 vs 3.33 +/- 0.32, p < 0.05 and 3.19 +/- 0.32 vs 3.21 +/- 0.29 p > 0.1, LF 3.41 +/- 0.33 vs 31.49 +/- 0.30 and 3.52 +/- 0.30 vs 3.61 +/- 0.32, p < 0.05, ANOVA). The differences were observed despite adjustment for age, sex and RRI. When fResp was added as covariate they became not significant. CONCLUSION: Patients with left ventricular dysfunction had faster rate of respiration. This finding may explain, in part, reduced HRV in these patients. The rate of respiration should be taken into account for correct interpretation of HRV analysis.
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In the paper two cases are described of patients in whom during angiography coexistent occlusion of the left descending artery and left circumflex artery was found. ECG and echocardiography in both cases were not indicating such a high coronary vessel defect. In both patients angiography was performed leading in one case to development of shock with fatal outcome.
Thirty patients with hypertrophic cardiomyopathy (HCM), (20 men and 10 women, age 16-55, mean 37 +/- 8 years) underwent exercise test done on bicycle twice to estimate effort tolerance before drugs. In all patients a 24-hour ekg Holter monitoring was also performed. During exercise test heart rhythm disturbances were noticed in 2 patients (7%). One had a 2-second sinus arrest, in the other ventricular bigeminity was observed. Twenty two patients (79%) had rhythm or conduction disturbances in Holter monitoring. In 2 (7%) rhythm generation and conduction abnormalities, in 7 (23%)-supraventricular and in 13 (43%)-ventricular arrhythmia. Ten of them (33%) had Lown class IVa and IVb arrhythmia. In conclusion we suggest that exercise test done on bicycle ergometer is a safe method to estimate effort tolerance in patients with HCM and usually does not induce rhythm disturbances. Holter monitoring is more effective than exercise test in revealing cardiac arrhythmia.
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Immediate effect of PTCA and CABG for unstable angina then followed-up for PTCA and CABG several years are analyzed in 112 patients selected out of 204 unstable angina patients hospitalized from 1990 to 1991. Fifty three patients, aged 25-68 (mean 51) were assigned to PTCA, fifty nine aged 33-69 (mean 53) were subjected to CABG. Both groups comprised of 72% and 83% males respectively. Nine patients with de novo angina, forty with crescendo angina and four with prolonged stenocardia were assigned to PTCA. 28% of patients have had myocardial infarction. Nine patients with de novo angina and fifty with crescendo angina were assigned to CABG. 56% of them have had myocardial infarction. Left ventricular ejection fraction (LVEF) less than 40% was found in 8 (15%) PTCA patients and in 18 (31%) patients who underwent CABG. Full revascularization was achieved in 38 (73%) patients treated with PTCA and 46 (78%) CABG patients. In 9/17% patients only critical stenosis in multivessel disease was subjected to PTCA. Four cases of myocardial infarction underwent intervention and all of these patients died: one (2%) after PTCA, and three (5%) after CABG. Fifty two patients after PTCA and fifty six after CABG were followed for one to four (mean 3) years. Thirty one percent of patients after PTCA and 41% after CABG were asymptomatic, 61% and 54% respectively had little to moderate symptoms. Left ventricular systolic function improved in most patients, predominantly in those with LVEF less than 40% (p < 0.05) treated with PTCA. Hospitalization due to anginal pain was needed in 46% of patients after PTCA and 15% after CABG (p < 0.05). Coronary artery restenosis after PTCA was successfully treated with re-PTCA or CABG in 9 (17%) patients. Venous graft stenoses were dilated in two cases. Myocardial infarction occurred in 3 (6%) patients after PTCA and 2 (4%) patients after CABG. One patient died after redilatation CABG treated patients required nonsignificantly less antianginal drugs. Four week survival rate in PTCA group and CABG group was 98% and 95% respectively; three year survival was 95% in both groups. We conclude, that unstable angina patients requiring either angioplasty or surgery may expect good procedural and long term prognosis. Remarkably good results may be expected in successfully revascularised patients with low ejection fraction.
The study was performed in 18 patients (15 F and 3-M) aged 35-57 yers (mean 46 +/- 7) diagnosed as idiopathic lung fibrosis. Ten patients (group A) recived standard treatment (prednisone 10-15 mg/day) and supplementary home oxygen therapy (mean 16.4 h/day) for a period of 4 years. During exacerbations antibiotics, theophylline and expectorants were prescribed. Eight patients (group B) receiving the same treatment without home oxygen, served as controls. At study entry lung function test (TLC, VL, Dlco), blood gases, hematocrit, hemodynamic parameters of the pulmonary circulation and thermodilution cardiac output were measured in all patients. The measurements were repeated after 4 years of follow-up. At follow-up examination no differences in pulmonary function parameters were shown between the groups. Mean pulmonary artery pressure and pulmonary vascular resistance were significantly lower in patients receiving home oxygen therapy (group A) as compared with those treated pharmacologically only (group B). Best effects of oxygen therapy were observed in patient with lower pulmonary artery pressures at study entry.
The aim of this study was to assess the effect of chronic home oxygen therapy on cardiac function in patients with idiopathic interstitial lung fibrosis. Ten patients (Group A) received standard pharmacological treatment (prednisone 10-15 mg/day) and supplementary home oxygen therapy (mean 16.4 h/day) for the period of 4 years. Eight patients (Group B) received pharmacological treatment alone for the same period of time. Left ventricular ejection fraction was measured with a scintillation probe. Right and left ventricular function was also assessed by means of echocardiography. All measurements were taken at the beginning of study and repeated at the end of the 4 year follow-up. Anatomical and functional deterioration was slower in group A than in group B. Statistically significant differences between the groups at follow-up were found with respect to the right ventricle-early inflow velocity and tricuspid E/A ratio. Changes in left ventricular function were also different between the groups. A significant decrease in ejection fraction and mitral E/A ratio was observed in group B, while the corresponding changes in group A were not significant. These results suggest that chronic home oxygen therapy attenuates cardiac dysfunction in patients with idiopathic interstitial lung fibrosis.
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We studied the correlation between changes in left ventricular filling dynamics induced by acute intravenous administration of verapamil and the changes in exercise tolerance induced by oral administration of the agent in 30 patients with hypertrophic cardiomyopathy. Diastolic cardiac function was measured by means of a nuclear stethoscope before and 10 min after intravenous administration of verapamil, 0.15 mg.kg-1 over 2 min. Treadmill exercise tests using a modified Bruce protocol were performed before the initiation of oral verapamil treatment and after 4 weeks of oral therapy at a dose of 320-360 mg.day-1 (mean +/- SD 332 +/- 17 mg.day-1). Peak filling rate (PFR) increased in 21 patients, 18 of whom (86%) also had an increase in exercise duration, PFR showed no increase in nine patients, eight of whom (89%) had no change in exercise duration (sensitivity 95%, specificity 73%, predictive value of the positive result 86%, predictive value of the negative result 89%). Acute changes in time from the beginning of rapid filling to PFR (t-PFR) and in left ventricular end-diastolic volume (EDV) were less useful in predicting improvement in exercise tolerance. In 19 patients the changes in PFR and EDV paralleled. Twelve of the 13 patients (92%) with an increase in both parameters also had an increase in exercise duration, whereas all six in whom these parameters were reduced showed no increase in exercise duration (sensitivity 100%, specificity 86%, predictive value of positive results 92%, and predictive value of negative results 100%).(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of sotalol on exercise tolerance and incidence of arrhythmias was studied in 30 patients with hypertrophic cardiomyopathy (HCM). In this short-term, double-blind, cross-over study, exercise time on sotalol (320 mg/day) was significantly longer than on placebo (10.6 +/- 4.0 vs. 9.4 +/- 3.6 min; p < 0.01). Sotalol eliminated supraventricular arrhythmias in 6 of 7 patients (p < 0.03) and suppressed ventricular arrhythmias in 7 of 13 patients in whom they were present on placebo (p < 0.05). Ventricular tachycardia was abolished in 4 of 8 patients, but appeared during sotalol treatment in 1 patient who was free of repetitive arrhythmias on placebo. Twenty-five patients who had better exercise tolerance on sotalol than on placebo and did not experience aggravation of arrhythmia entered a 6-month prospective, open-label treatment with sotalol (160-480 mg/day, mean +/- SD 377 +/- 94). One patient was withdrawn after 1 month because of bronchospasm. Mean exercise time improved from 9.8 +/- 3.6 min on placebo to 12.7 +/- 3.2 min (p < 0.01) after 6 months of treatment with sotalol. During the prospective follow-up, sotalol abolished ventricular tachycardia in all 6 patients after 1 month (p = 0.022), and in 4 of 6 patients (p > 0.2) after 6 months of treatment. It is concluded that sotalol significantly improves exercise tolerance and is effective in suppressing both supraventricular and ventricular arrhythmias in patients with HCM.
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The aim of this study was to compare two different quantitative methods used to determine left ventricular regional wall motions. Circumferential and radial methods were used to distinguish between normo- and hypokinesia of the 5 segments proposed by AHA for RAO position. One hundred ventriculograms were analyzed. Fifty cases with normal wall motion and ejection fraction greater than 55% were chosen as a base to enumerate normokinetic values of regional contractility. The other fifty cases represented hypokinesia of different segments. Respective values for the radial method were 61.42 vs 38.10 for antero-basal segment, 73.8 vs 58.5 for antero-lateral segment, 67.74 vs 42.5 for apical segment, 69.88 vs 47.70 for postero-lateral segment and 41.72 vs 33.4 for postero-lateral segment. The values obtained with the circumferential method were 12.27 vs 10.21, 20.06 vs 16.21, 22.19 vs 18.78, 17.08 vs 11.39 and 8.50 vs 8.15, respectively. These results suggest that the radical method allows to better differentiate between hypo- and normokinesia. Postero-basal segment proved to be most difficult to assess. Both methods fail to make a clear distinction in these cases.
In a group 26 patients with hypertrophic cardiomyopathy the values of certain polycardiographic and haemodynamic indices and their changes in the prolongation of the time of isovolumetric relaxation (IVRT) was noted in 23 patients (88%), with increased value of the percent of the a wave participation of the apexcardiogram (%a) in 24 patients (92%). In the obstructive type the corrected time of left ventricular ejection was significantly prolonged (p < 0.01) in relation to the non-obstructive type. No difference was observed in the values of these parameters depending on the functional class. A weak but significant correlation was demonstrated between the %a and the end-diastolic left ventricular pressure (r = 0.579, p < 0.01). The IVRT value showed an increasing tendency in this prospective study, particularly in patients with progression of clinical symptoms.
In 75 patients with hypertrophic cardiomopathy (HCM) followed for a mean period of 5.5 years (range 2-20 years), evolution of the electrocardiographic (EKG) changes was assessed. Progression of EKG abnormalities occurred in 35 patients (47%). It was manifested by an increase in precordial QRS voltage in 33 patients, development of new P-wave mitral in 11 patients, and development or disappearance of pathologic Q waves in 14 patients. With follow-up times greater than 5 years, 5-8 years, and greater than 8 years, EKG progression was present in 27, 41, and 80% of patients, respectively. Age less than 30 years at the beginning of study and left ventricular outflow obstruction predisposed to EKG progression within 5-8 years. Patients with progressive EKG changes were more prone to experience clinical deterioration than those without EKG progression (63 vs. 15%, p less than 0.001). With chronic verapamil administration, progression of EKG abnormalities occurred insignificantly less often than with propranolol treatment (35 vs. 64%, p = 0.20). It is concluded that with long-term follow-up, HCM tends to progress in a significant proportion of adult patients.