Heart and vessels. Supplement最新文献

Increased plasma catecholamines - in particular, excessive beta-adrenoceptor activation in chronic heart failure - may easily desensitize the beta-adrenoceptors as well as the postreceptor signal transductions. Since these detrimental changes in the failing heart could be reversible, administration of low-dose beta-blocker, which minimizes the negative inotropic effects, may be effective in attenuating the harmful effects of sympathetic nerve activation. Beta-adrenoceptor stimulation may also produce microtubule disruptions of the cell either through direct action or through an increase in heart rate. Treatment with beta-blockers could attenuate Ca overload by slowing the heart rate and may be useful as a protection from the structural disintegration of the cell. Thus, to clarify the underlying mechanisms of beta-blocker therapy for chronic heart failure, we have to consider not only to the functional aspects but also to the structural changes of the cells.

The effect of beta-blockade in dilated cardiomyopathy was studied by a questionnaire survey. Thirty-three cases were monitored in whom metoprolol (22 patients, 35.9 +/- 20.4 mg, mean +/- SD), propranolol (four patients, 26.3 +/- 7.5 mg), or other beta-blockers (seven patients) were administered. Four patients died, but no direct relationship was found between administration of beta-blocker and death. The NYHA functional class improved significantly. The mean heart rate decreased from 96/min to 77/min (P less than 0.01). The mean cardiothoracic ratio decreased from 55.6% to 52.1% (P less than 0.01). The mean ejection fraction of the left ventricle measured by echocardiogram increased from 30.4% to 36.9% (P less than 0.01). Exercise tolerance in the treadmill test improved significantly. There was no change in blood pressure, nor were there arrhythmias seen on Holter electrocardiograms. In two patients, congestive heart failure deteriorated after administration of beta-blockers. It is concluded that beta-adrenergic blockade has a beneficial effect in most of the patients with dilated cardiomyopathy.

Conventional therapy of patients with idiopathic dilated cardiomyopathy is currently directed at the control of heart failure. However, the morbidity and mortality of idiopathic dilated cardiomyopathy remains very high despite such interventions. One promising new approach to therapy of idiopathic dilated cardiomyopathy is beta-blockade. The potential mechanisms for benefit from beta-blockade include protection from catecholamine cardiotoxicity, upregulation of myocardial beta-adrenergic receptors, reduction in sudden death, reduction in heart rate, improved ventricular diastolic function, and reduction in afterload. Several reports have suggested that long-term beta-blockade may improve hemodynamic function, clinical symptoms, and survival in patients with idiopathic dilated cardiomyopathy. However, data from controlled trials are limited and some reports have been negative. This paper will summarize the rationale for the use of beta-blocker therapy in idiopathic dilated cardiomyopathy and review the clinical experience with this therapy.

Beta-blockers were initially given to patients with chronic heart failure due to ischemic heart disease and resting tachycardia. The prompt effect on severe backward heart failure was directly associated with an immediate fall in heart rate. This observation led to long-term administration to patients with idiopathic dilated cardiomyopathy and, later, to patients with ischemic cardiomyopathy and secondary cardiomyopathies as well. Due to marked down-regulation of beta receptors, patients with heart failure are extremely sensitive to beta blockade. A test dose of metoprolol 5 mg b.i.d. for 2 days is recommended to select patients for long-term beta-blockade, followed by careful titration with increment in dose over 6 weeks. One important effect of beta-blockade in the early phase of treatment is a reduction in the myocardial energy demand early after the onset of long-term treatment. After 1 month of treatment with beta-blockers, marked improvement of diastolic function is observed. This effect might be attributed to inhibition of calcium overload. After 3 months of treatment, an increase in ejection fraction can be observed, which might be attributed to upregulation of beta receptors. The withdrawal of long-term treatment was followed by a deterioration of heart function in 61% of patients and improvement was seen after reinstitution of beta-blockade. There was an increase in cardiac index and stroke work index at rest as well as during supine exercise. A marked fall in left ventricular filling pressure at rest and unchanged filling pressure during supine exercise was noted, while exercise capacity increased by 25%. A similar pattern was seen in patients with ischemic cardiomyopathies and other secondary cardiomyopathies. However, the increase in ejection fraction in the ischemic cardiomyopathy group was lower (0.06) compared to the groups with dilated cardiomyopathy and other secondary cardiomyopathies (0.18).

The relation between myocardial histological changes and ventricular tachycardia (VT) in cardiomyopathy was investigated. Right ventricular endomyocardial biopsy and 24-hour ECG-monitoring were performed in 19 patients with dilated cardiomyopathy (DCM) and 22 with hypertropic cardiomyopathy (HCM). Cardiomyopathy was histologically divided into the following four groups: group A, hypertrophy without disarray of myocytes (3 DCM and 7 HCM); group B, hypertrophy with disarray of myocytes (14 HCM); group C, fibrosis (9 DCM and 1 HCM); and group D, diffuse myocytic degeneration (7 DCM). VT was observed in 20% (2 of 10 patients) of group A, 14% (2 of 14) of group B, 80% (8 of 10) of group C, and 71% (5 of 7) of group D. The degenerating myocytes and/or the irregular distribution of fibrosis may play an important role in the etiology of VT in cardiomyopathy.

Two autopsied cases clinically compatible with arrhythmogenic right ventricular dysplasia were pathologically examined. Residual cell infiltration and irregular adipofibrosis suggested a pathogenesis of chronic myocarditis in these cases.

A case with arrhythmogenic right ventricular dysplasia involving the left ventricle as well as the right ventricle was presented. Right ventricular endomyocardial biopsy and computerized tomography were useful in detecting fatty tissue in the myocardium. This case deserves to be reported in reference to detecting fatty tissue in arrhythmogenic right ventricular dysplasia by using computerized tomography.

Fifteen patients with right ventricular tachycardia without evidence of coronary artery disease or dilated or hypertrophic cardiomyopathy were evaluated, by means of electrophysiologic study and right ventricular endomyocardial biopsy. Six cases were diagnosed as definite arrhythmogenic right ventricular dysplasia (ARVD), while 2 cases without characteristic findings of ARVD by noninvasive studies and angiography were diagnosed as probable ARVD on the basis of their electrophysiologic and histopathologic data. In conclusion, ARVD is relatively common as an etiology of right ventricular tachycardia, and detailed electrophysiologic study and endomyocardial biopsy appear to be useful for diagnosis of ARVD.