The right ventricle in congenital heart disease

In patients with congenital heart disease the right ventricle (RV) may support the pulmonary (subpulmonary RV) or the systemic circulation (systemic RV). During the last 50 years evidence is accumulating that RV dysfunction develops in many of these patients and leads to considerable morbidity and mortality. Therefore RV function in certain groups of congenital heart disease patients needs close surveillance and timely and appropriate intervention to optimise outcomes. Despite major progress being made, assessing the RV either in the subpulmonary or the systemic circulation remains challenging, often requiring a multi-imaging approach and expertise (echocardiography, magnetic resonance imaging, nuclear and occasionally invasive assessment with angiography). This review discusses the implications of volume and pressure loading of the RV in the context of congenital heart disease and describes the most relevant imaging modalities for monitoring RV function.     

Aortic atresia with a solitary and indeterminate ventricle

A male infant having aortic atresia and double inlet to a solitary and indeterminate ventricle, presented a clinical picture of "hypoplastic left heart syndrome". Haemodynamic consequences are described and comparison made to other types of aortic atresia. Cross-sectional echocardiography was found to be reliable in determining both atrioventricular and ventriculo-arterial connections in the presence of aortic atresia and a solitary ventricle.     

The right ventricle in congenital heart disease.

An increasing number of children with congenital heart disease are surviving into adulthood, creating new, unusual patients with different physiologic and anatomic problems for the adult cardiologist. This article discusses those lesions affecting primarily the right ventricle.     

Diastolic filling of the heart ventricle

It is demonstrated that negative, "subatmospheric" pressure developing in the heart ventricles during the rapid-filling phase is an evidence of active diastole and inflated capacity of heart chambers. Diastolic activity of the heart increases as a result of insufficient blood inflow to the ventricles coupled with inadequate venous return or narrowed atrioventricular orifice. It is assumed that the heart's diastolic activity is an adaptive-compensatory mechanism adequately stabilizing circulation under changing hemodynamic conditions.     

The heart (ventricle and atrium) is the heart of hypertension, not blood pressure

Some old icons of hypertension warrant questioning in view of new insights. Lowering of blood pressure is no criterion of efficacy in prevention of cardiovascular morbidity, mortality and sudden death. The drugs used in early studies - diuretics, vasodilators and reserpine - greatly improved mortality from malignant hypertension, apoplectic stroke and congestive heart failure, but had little or no effect in persons with milder degrees of elevated blood pressure, who constitute the vast majority of hypertensives. The failure of diuretics and vasodilators to influence cardiovascular disease favorably appears due not to their known adverse effects on risk factors, such as lipids, as some have held, but to a failure - in conjunction with some sympathetic blocking agents - to cause effective regression of left ventricular hypertrophy, the keystone of successful therapy. A study of 674 hypertensive persons surveyed in the United States and eastern Canada, personally examined during their visit to a Florida health resort, has shown striking changes in prescribing practice during the period surveyed (1985-88), notably with increased use of angiotensin converting enzyme (ACE) inhibitors and, to a lesser degree, increased use of calcium channel blockers. Both of these cause regression of left ventricular hypertrophy, and will hopefully show long term benefit in decreasing hypertension mortality. Left ventricular hypertrophy is detected most sensitively echocardiographically, and is worthwhile not only for estimation of prognosis, but also for guiding therapy. Left atrial hypertrophy is a mirror of left ventricular hypertrophy and may be detected echocardiographically and in the electrocardiogram.(ABSTRACT TRUNCATED AT 250 WORDS)     

Importance of the right ventricle in valvular heart disease

The importance of the right ventricle as a determinant of clinicalsymptoms, exercise capacity, peri-operative survival and postoperativeoutcome has been underestimated for a long time. Right ventricularejection fraction has been used as a measure of right ventricularfunction but has been found to be dependent on loading conditions,ventricular interaction as well as on myocardial structure.Altered left ventricular function in patients with valvulardisease influences right ventricular performance mainly by changesin afterload but also by ventricular interaction. Right ventricularfunction and regional wall motion can be determined with rightventricular angiography, radionuclide ventriculography, two-dimensionalechocardiography or magnetic resonance imaging. However, thecomplex structure of the right ventricle and its pronouncedtranslational movements render quantification difficult. Trueregional wall motion analysis is, however, possible with myocardialtagging based on magnetic resonance techniques. With this techniquea baso-apical shear motion of the right ventricle was observedwhich was enhanced in patients with aortic stenosis.     

The pattern of intramural veins of the left ventricle of the human heart.

A detailed injection, microradiographic, and histological necropsy study of 18 hearts showed that the pattern of myocardial veins differed from the arterial pattern. In "normal" hearts, large drainage veins began in the subendocardial zone and coursed fairly directly towards the epicardium, maintaining a comparatively even calibre throughout. Smaller, but similar, drainage veins also begain in the middle of the myocardial wall. In the outer myocardium small groups of these vessels converged to form a single vein which then entered, almost at right angles, the pericardial veins. In general, small veins within the myocardium entered directly into the large drainage veins without any extensive intermediate sized venous network. In "abnormal" hearts with left ventricular hypertrophy the myocardial veins appeared basically normal but were more widely separated and consequently overall less dense on microradiography. Interruption of main drainage veins and loss of normal pattern were seen in areas of myocardial fibrosis associated with coronary artery disease. In a heart with severe generalized coronary artery atheroma the normal pattern in the inner half of the wall was replaced by a "plexus" of small veins in which the majority of vessels coursed circumferentially. The possible significance of both the normal and abnormal vein pattern is discussed.     

Right ventricle in patients after orthotopic heart transplantation

Eighteen patients were examined by echocardiography one month before, and one month after orthotopic heart transplantation (OHT). The right-heart echocardiographic parameters were compared with pulmonary haemodynamics. All recipients showed increased mean pulmonary artery pressure (PAP) (42 +/- 8 mmHg) and pulmonary vascular resistance 3.0 +/- 1.3 u.) before OHT. The causes of the pulmonary hypertension, and indications for OHT, were the end stage of dilated cardiomyopathy (n = 8), ischaemic heart disease (n = 9) and aortic valve disease (n = 1). After transplantation, the donor's right ventricle dilates due to the recipient's elevated pulmonary vascular resistance. The right ventricular dimension after OHT was greater than 30 mm in 1/3 of patients. The right ventricular diastolic dimension correlates statistically significantly with mean PAP of the recipient before the procedure. Right ventricular dilatation is accompanied by a mild degree of tricuspid insufficiency (in 89% of cases), as documented by Doppler examination. Neither the degree of right ventricular dilatation, nor the degree of tricuspid insufficiency show a tendency to progression during follow-up.     

冠心病的危险分层

冠心病的基础病变为动脉粥样硬化，在其进展过程中可因易损斑块破裂导致血小板聚集和血栓形成，发生急性冠状动脉综合征（acute coronary syndrome，ACS）。ACS的临床表现可以是不稳定型心绞痛（unstable angina pectoris，UAP），也可以是大面积心肌梗死甚至猝死。冠心病预后差异很大。根据冠心病预后的因素，综合临床资料判断预后，制定治疗策略，都涉及冠心病危险分层。     

Programmed noninvasive stimulation of the heart ventricle transcutaneously]

Possibility of performing of a programmed transcutaneous heart stimulation by combining two, easily purchasable noninvasive cardiac stimulators was examined in 4 healthy volunteers. Combining of a SP-5 transesophageal stimulator with a transcutaneous NP-4D stimulator made conduction of the programmed cardiac stimulation possible as well as two undisturbed ECG recordings. The quality of the obtained recordings (surface and transesophageal) made estimation of the retrograde AV conductivity possible. The performed examinations point out to a practical utility of the applied combination of transesophageal and transcutaneous stimulation-for conducting of noninvasive diagnostic heart examination.     

The effect of cardiac sympathetic nerve stimulation on the right ventricle in canine heart

The change in coronary hemodynamics during right or left cardiac sympathetic nerve stimulation was studied in anesthetized open chest dogs. No difference in the increasing rate of mean coronary blood flow between right coronary artery (RCA) and left anterior descending coronary artery (LAD) was observed. However the increasing rate of right ventricular systolic pressure X heart rate (RVSP X HR) was greater than that of left ventricle (LV). With phentolamine injection, cardiac sympathetic nerve stimulation showed similar changes as the controls. Beta-stimulation by isoproterenol infusion did not cause different effects on the increasing rate of coronary blood flow between RCA and LAD. These results showed that cardiac sympathetic nerve stimulation increased the double product of the right ventricle (RV) more than that of the LV and the increase was not affected by phentolamine. Moreover, cardiac sympathetic nerve stimulation, either the right or the left, caused the greater effects on the RV compared to the LV mainly through beta-adrenoceptors, and that the response of the RV to increase in oxygen demand was possibly, in part, different from that of the LV.