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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, the acute hemodynamic effects of pimobendan (2.5 mg), a new drug, was compared with that of captopril (12.5 mg) in the same 8 patients with chronic heart failure (NYHA class II-III); 3 with dilated cardiomyopathy and 5 with regurgitant valvular heart disease. The hemodynamics were serially assessed before and after drug administration for at most 6 hours. Pimobendan reduced mean blood pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure, right atrial pressure, total systemic vascular resistance, and total pulmonary vascular resistance but it increased heart rate. By contrast, captopril reduced mean blood pressure and double product. No significant changes were noted in the cardiac index, stroke volume index, AV-O2 difference or the arterial oxygen pressure between the 2 drugs. In conclusion, pimobendan seems to function as a strong arterio-veno-dilator rather than as an inotropic agent in patients with chronic heart failure.
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PMID:[Acute hemodynamic effects of pimobendan and captopril: a comparative study in the same patients with chronic heart failure]. 134 39

Mitral or tricuspid regurgitation of long duration may so shorten the ventricular filling time in dilated cardiomyopathy that stroke volume is limited. We assessed the effects of changing the atrioventricular interval during temporary or permanent dual-chamber DDD pacing in twelve dilated cardiomyopathy patients with short ventricular filling times due to regurgitation. We measured ventricular filling time and cardiac output with doppler echocardiography and exercise capacity on a treadmill, at baseline and with the best atrioventricular delay during pacing. The durations of both mitral and tricuspid regurgitation were significantly shorter at the shorter atrioventricular interval (mean reductions 85 [95% CI 60-110] ms and 110 [75-150] ms, respectively; p < 0.001 for both). There were consequent increases in left-ventricular and right-ventricular filling times (65 [35-95] ms and 90 [60-120] ms, p < 0.001). For each 50 ms reduction in atrioventricular delay, left-ventricular filling time increased by 35 ms in six subjects with presystolic mitral regurgitation and right-ventricular filling time by 30 ms in nine subjects with presystolic tricuspid regurgitation. At the short atrioventricular interval, cardiac output was greater than baseline (by 1.1 [0.8-1.4] l/min, p < 0.01) and there were rises in exercise duration (104 [45-165] s, p < 0.05) and maximum oxygen consumption (2.1 [1.5-2.7] ml kg-1 min-1, p < 0.05). There was a decrease in the Likert visual analogue score of breathlessness at peak exercise (8.6 [SD 2.1] vs 4.9 [3.1], p < 0.01). Although from a small sample, these findings suggest that DDD pacing with a short atrioventricular delay may have therapeutic potential in patients with dilated cardiomyopathy, even in the absence of conventional indications for pacemaker implantation.
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PMID:Effects of dual-chamber pacing with short atrioventricular delay in dilated cardiomyopathy. 809 51

Congestive heart failure (CHF) is a common manifestation of hypertension, coronary artery disease, and dilated cardiomyopathy. The Framingham study showed that the incidence of CHF increases twofold with each decade of age. The presence of CHF increases the age-adjusted death rate 5.5-fold for women and 8-fold for men, and it increases the sudden death rate 5.5-fold in both men and women. Ventricular arrhythmias are a common accompaniment of CHF. Ambient ventricular premature complexes occur in most of these patients, and nearly one half of all CHF patients will have nonsustained ventricular tachycardia on a 24-h ambulatory electrocardiographic (Holter) recording. In addition, low left ventricular ejection fraction (LVEF) predicts inducible sustained ventricular tachycardia on electrophysiologic study. One-year mortality increases with worsening New York Heart Association (NYHA) Functional Class and decreasing LVEF. As the overall yearly mortality increases, the proportion of patients who die of arrhythmias decreases. The precise mechanism of death is frequently difficult to assess. Nonarrhythmic causes of death include CHF, shock, electromechanical dissociation, and myocardial rupture. Arrhythmic causes are most commonly due to ventricular tachycardia/ventricular fibrillation. Bradycardic events (asystole or heart block) are usually associated with progressively worsening CHF. Noncardiac causes that may confuse classification include pulmonary embolus and cerebrovascular accident. Because many patients have ischemic heart disease as the etiology of the CHF, a recurrent ischemic event can likewise make classification difficult. Overall, approximately one half of all deaths in CHF are arrhythmic and one half are nonarrhythmic.
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PMID:Clinical significance and management of arrhythmias in the heart failure patient. 139 10

Deletions and point mutations of mitochondrial DNA (mtDNA) of patients with dilated or hypertrophic cardiomyopathy were analyzed using the polymerase chain reaction and fluorescence-based direct sequencing. The patients included are with hypertrophic cardiomyopathy associated with left ventricular dilatation, a patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and a patient with fatal infantile cardiomyopathy. Deletions were frequently seen in mtDNA in patients with dilated cardiomyopathy. The mtDNA was sequenced and the direct repeat at each edge of deletion was identified as (5'-CATCAACAACCG-3') which was located in the ATPase6 gene and in the D-loop region. In a patient with hypertrophic cardiomyopathy associated with left ventricular dilatation, another mutant mtDNA was found not to have directly repeated sequence, and was revealed to jump from nucleotide position 8,992 to position 16,072 of mtDNA resulting in a 7,079 bp deletion. This patient had unique point mutation in the tRNA genes. A G-to-A transition in the tRNA(Cys) gene (nucleotide position 5,821) at the aminoacyl acceptor stem and an A-to-G transition in the tRNA(Thr) gene (nucleotide position 15,951) were identified. In a patient with MELAS, an A-to-G transition in the tRNA(Leu)(UUR) gene (nucleotide position 3,243) was observed. This mutation was located at the 5' end of the dihydrouridine loop of this tRNA molecule, and would disturb its function. In a patient with hypertrophic cardiomyopathy associated with lactic acidosis, mutations of mtDNA should be suspected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitochondrial DNA mutations in cardiomyopathy. 143 21

To analyze right-ventricular size and function and their relationship to left-ventricular dimensions in patients with dilated cardiomyopathy (DCM), biplane cineventriculography was performed in 57 patients. The results were compared to 15 normals (N). In patients dilatation of the right ventricle (RVEDVI: DCM: 126.5 +/- 41.4 ml/m2, N: 90.5 +/- 9.2 ml/m2, 2 p < 0.05) was less pronounced than dilatation of the left ventricle (LVEDVI: DCM: 136.0 +/- 45.8 ml/m2, N: 76.7 +/- 7.9 ml/m2, 2 p < 0.05). Left-ventricular ejection fraction (LVEF: DCM: 36.1 +/- 10.2%, N: 64.4 +/- 3.8%, 2 p < 0.05) was more reduced than right-ventricular ejection fraction (RVEF: DCM: 39.7 +/- 11.5%, N: 58.3 +/- 3.3%, 2 p < 0.05). Concerning the individual patient, a good correlation was found between right- and left-ventricular stroke volume (r = 0.74), whereas ejection fraction (r = 0.58), enddiastolic (r = 0.52) and endsystolic volume (r = 0.55) of the left and right ventricle correlated only moderately. Twenty-three of the 57 patients showed pronounced differences between right- and left-ventricular ejection fraction. The difference RVEF-LVEF was < = -10% in six patients, i.e., right-ventricular ejection fraction was markedly more reduced than left-ventricular ejection fraction. Right-ventricular myocardial biopsy was performed in five of these six patients with histologic evidence of dilated cardiomyopathy and, also, no signs of right-ventricular dysplasia (no lipomatous tissue replacement).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Function of the right ventricle in patients with dilated cardiomyopathy]. 144 96

The influence of heart rate (HR) and AV delay (AVD) on left ventricular haemodynamics was studied in 12 patients classified as having coronary heart disease (CHD), hypertensive heart disease (HHD), dilated cardiomyopathy (DCM) or who served as controls. Using the conductance catheter technique, haemodynamics were measured during pacing rates of 80 to 180 beat.min-1 at AV delays of 0 to 240 ms. A 3-D linear regression analysis of the data quantified the influence of HR and AVD in principle for each group. An increase in HR resulted in a rise in the cardiac index without changing ejection fraction in the control group only, but led to a decrease in these parameters in HHD and DCM; cardiac index remained constant in CHD. CHD patients frequently had a more pronounced left ventricular end-diastolic pressure (LVEDP) elevation with higher HR, whereas left ventricular end-diastolic volume (LVEDV) and stroke volume decreased. In patients with HHD, lengthening of the AVD resulted in an increase in LVEDV and a decrease in LVEDP and left ventricular end-systolic volume (LVESV) leading to a higher ratio of stroke volume to LVEDP than in the other subsets. In DCM, longer AVD also resulted in a higher SV/LVEDP ratio, but in contrast to HHD the influence of AVD variation on LVEDP and therefore on the LVEDV/LVEDP ratio was missing.
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PMID:Ventricular performance in relation to heart rate and AV delay at rest. 147 17

The effects of unloading or inotropic agent in 22 patients with dilated cardiomyopathy were assessed in terms of optimal coupling between the ventricle and arterial system. In 13 patients (group A), lower body negative pressure (LBNP) was applied to reduce preload and nitroprusside was used to decrease afterload. In 9 patients (group B), dobutamine was used to enhance inotropic state. In all patients, the direct arterial pressure was simultaneously recorded with left ventricular echocardiogram as the pressure was elevated by phenylephrine. The left ventricular contractile properties were defined by the slope (Ees) of the end-systolic pressure-volume relation. The arterial system properties were expressed by the slope (Ea) of the end-systolic pressure-stroke volume relation. When the Ea/Ees ratio ranged from 0.5 to 1.0, both external work and mechanical efficiency are nearly maximized. In group A, baseline ventricular-load coupling was characterized by an increase in the Ea/Ees ratio (1.96 +/- 1.08) where the heart could maximize neither external work nor mechanical efficiency. Ea/Ees significantly fell to 1.45 +/- 0.77 with nitroprusside, while increasing to 2.37 +/- 1.17 during LBNP. In group B, Ea/Ees was decreased from 1.43 +/- to 0.82 +/- 0.47 with dobutamine. It is concluded that reduction in afterload rather than preload, or augmentation of contractility could restore optimal ventricular-load coupling in patients with severe cardiac dysfunction.
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PMID:Ventricular-load optimization in patients with heart failure. 149 65

Recent experimental studies have shown that cardiomyoplasty using the right latissimus dorsi provides excellent hemodynamic augmentation. Based on these experimental findings, this procedure was performed in a 40-year-old man with a dilated cardiomyopathy after a large myocardial infarction. The patient tolerated the procedure well and has had marked functional improvement. Examination 6 months after operation demonstrated decreases in right atrial pressure, pulmonary capillary wedge pressure, and left ventricular end-diastolic volume. In addition, increases were noted in cardiac output, stroke volume, left ventricular stroke-work, right ventricular ejection fraction, and left ventricular ejection fraction. Because of this promising clinical result, we have started a series of right latissimus dorsi cardiomyoplasties for left ventricular failure.
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PMID:Right latissimus dorsi cardiomyoplasty for left ventricular failure. 159 42

Sixteen patients with dilated cardiomyopathy were examined hemodynamically in order to clarify the relationship between the exercise capacity and the effects of afterload reduction at rest using supine graded bicycle exercise testing before and after sublingual administration of 10 mg nifedipine. 1) The integration of work loads was weakly correlated with the stroke index (r = 0.64), heart rate (r = -0.58) and plasma norepinephrine concentration at rest (r = 0.49), but not with the left ventricular ejection fraction, cardiac index, pulmonary arterial diastolic pressure or the mean arterial pressure at rest. 2) Changes in stroke index and heart rate after administration of nifedipine correlated well with the integration of work loads (r = -0.84, r = 0.81, respectively). Thus, in patients with dilated cardiomyopathy changes in stroke volume and heart rate due to afterload reduction at rest were better predictors of exercise capacity than the baseline left ventricular hemodynamic parameters.
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PMID:Hemodynamic changes due to afterload reduction as a predictor of exercise capacity in patients with dilated cardiomyopathy. 161 Nov 85

Programmed electrical stimulation was performed in 12 patients with moderate to severe congestive heart failure and ventricular tachycardia (VT) to study possible arrhythmogenic properties of ibopamine, a new orally active dopamine agonist. Ibopamine induced no significant changes in spontaneous cycle length, PR, QRS, QTc, AH or HV intervals, and also right ventricular effective refractory periods were unaffected (for paced cycle lengths of 600 and 430 ms, respectively, using 1 extrastimulus: 287 +/- 16 ms at baseline vs 283 +/- 27 ms after ibopamine and 270 +/- 23 ms during the control study vs 262 +/- 19 ms after ibopamine). In 6 of the 8 patients with coronary artery disease but in none of the 4 patients with dilated cardiomyopathy, sustained VT was induced before and after ibopamine. Proarrhythmia was present in 1 patient, who became inducible after ibopamine. However, 1 patient had sustained VT only at baseline but not after ibopamine. The number of extrastimuli required for VT induction was equal (2.7 +/- 0.2 vs 2.7 +/- 0.2). Holter monitoring showed no changes in ventricular premature complexes, ventricular couplets and runs of VT after 1 week of ibopamine therapy. The signal-averaged electrocardiogram was abnormal in 11 and showed late potentials in 5 patients, but no changes occurred after ibopamine. During hemodynamic evaluation, increases in cardiac (32%) and stroke volume (34%) indexes were seen after administration of 100 mg of ibopamine, accompanied by a decrease in vascular resistance and filling pressures. Plasma norepinephrine decreased significantly after ibopamine (p = 0.02) but plasma epinephrine was unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrophysiologic profile of ibopamine in patients with congestive heart failure and ventricular tachycardia and relation to its effects on hemodynamics and plasma catecholamines. 168 46


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