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PubMed2002

[Right ventricular infarction: pathophysiology, diagnosis and treatment].

Acute right ventricular ischemia accompanies 40-80% of cases of infero-posterior myocardial infarction. Approximately one half of these patients present with hemodynamic compromise consisting of acute right ventricular failure, clear lungs and low cardiac output in spite of preserved left ventricular systolic function. The ischemic right ventricle appears to be relatively resistant to infarction and has remarkable ability to recover. Right ventricular performance improves spontaneously even in the absence of reperfusion, however reperfusion enhances this recovery and improves the clinical course of right ventricular infarction.

Humans↗
PubMed1989

Clinical correlates of acute right ventricular infarction in acute inferior myocardial infarction.

Right ventricular infarction was diagnosed on the basis of ST-segment elevation greater than or equal to 1 mm in at least one right precordial lead (V3R-V6R) in 20 of 50 patients with first acute inferior myocardial infarction. Seventy five percent of these had ST elevation in 2 or more right precordial leads. Giddiness and hiccups were more common amongst such patients (P less than 0.05). Signs of right ventricular dysfunction-raised jugular venous pressure (65%), Kussmaull's sign (45%), hypotension (without cardiogenic shock, 40%) and right-sided third sound (25%) in the absence of clinical left ventricular failure, were noted in 65% of such patients. Eleven patients had 2 or more of the above signs. ST elevation in 2 or more right precordial leads was found in 10 of these 11 patients. A more complicated course in the hospital characterised by bradyarrhythmias, hypotension and cardiogenic shock, combined with a greater mortality was seen in such patients. We conclude that the bedside diagnosis of haemodynamically significant right ventricular infarction can be made on the basis of a combination of clinical signs and ST elevation in 2 or more right precordial leads, even in units not equipped for bedside haemodynamic monitoring, echocardiography and radionuclide studies. This should lead to a better identification and management of such patients.

Acute Disease↗
PubMed2005

Early myocardial dysfunction following subarachnoid haemorrhage.

Like systolic dysfunction (SD), diastolic dysfunction (DD) has recently been proposed as a contributing factor in haemodynamic instability and in the genesis of pulmonary oedema, but its occurrence in subarachnoid haemorrhage (SAH) patients has not been described. Following aneurysmal SAH, three patients arrived at our institution with haemodynamic instability requiring vasoactive drugs and with pulmonary oedema. Transoesophageal echocardiographic study during aneurysm surgery documented mild to severe left ventricular SD and DD. Right ventricular SD and DD were also present. Documented biventricular systolic and diastolic myocardial dysfunctions may contribute to haemodynamic instability and pulmonary oedema following SAH due to intracranial aneurysmal rupture.

Adult↗
PubMed1991

Noncardiogenic mechanisms of right heart dysfunction.

Alterations in right ventricular (RV) performance are critical to the cardiac dysfunction witnessed in adult respiratory distress syndrome (ARDS), septic shock (SS), and as a consequence of positive end-expiratory pressure (PEEP) administration during mechanical ventilation. The authors review evidence for right heart dysfunction in these circumstances. In ARDS, an increase in RV afterload with the onset of pulmonary artery hypertension is the predominant factor promoting RV dysfunction. In SS, most investigators agree that a primary decrease in myocardial contractility is the major factor limiting RV performance. The application of PEEP during mechanical ventilation can potentiate alterations in RV preload, afterload, and/or contractility, all of which promote RV dysfunction and compromise left ventricular filling. As RV dysfunction may seriously affect global myocardial performance in all of these settings, the clinician must identify that RV function is impaired, discern the contributing mechanism, and select an appropriate therapeutic regimen targeted at addressing this predominant mechanism. Assessment and management strategies are described.

Critical Care↗
PubMed2004

Evidence of adverse ventricular interdependence in patients with atrial septal defects.

Right ventricular (RV) volume overload is associated with left ventricular (LV) distortion and dysfunction. The availability of transcatheter device closure of secundum atrial septal defect (ASD) provides an ideal model for investigating the immediate effects of elimination of RV volume overload and avoiding the confounding effects of surgery on LV function. Echocardiograms before and after device closure of ASD were analyzed for ejection fraction, percent changes in cross-sectional area and circumference, percent changes in free wall and septal endocardial lengths, and eccentricity. We enrolled 34 patients (median age 9 years) who underwent device closure of ASD (pulmonary to systemic shunt 1.6 +/- 0.4). Ejection fraction and LV end-diastolic volume, reflective of chamber preload, were significantly decreased in the presence of RV volume overload and normalized after defect closure with normalization of LV shape. Altered LV geometry secondary to RV volume overload was associated with regional variation in preload,such that diastolic circumference, a surrogate of myofiber preload, increased after closure of ASD secondary to a small increase in LV free wall arc length in conjunction with a much more significant increase in septal length. Thus, LV dysfunction associated with RV volume overload is secondary to altered chamber geometry and decreased myofiber preload. This physiology is immediately reversible and is independent of heart rate and afterload.

Child↗
PubMed1995

Pulmonary homograft insertion after repair of pulmonary stenosis.

Although the results of intracardiac repair for pulmonary stenosis or atresia are generally good, some patients develop symptoms due to to pulmonary regurgitation and right ventricular dilatation. Implantation of a pulmonary homograft may have a beneficial effect on these symptoms. Twenty-seven patients with symptoms due to pulmonary regurgitation and right ventricular dilatation were reoperated. The indication for surgery was dyspnea in 19, arrhythmia in five and both symptoms in three patients. The arrhythmia was supra-ventricular in four, ventricular in two and both supra-ventricular and ventricular in another two patients. A cryopreserved pulmonary homograft was implanted in the right ventricular outflow tract. Mean interval between intracardiac repair and homograft implantation was 15.6 years. Mean age at homograft implantation was 23.0 years. Concomitant procedures were performed in 18 patients. There were two early deaths (7%). Replacement of the homograft was necessary in one patient, 21 months after insertion. This patient had residual pulmonary stenosis immediately after surgery. On mid-term follow up (mean 36 months) all patients with dyspnea as indication for operation improved, except one with right and left ventricular dysfunction. Only two of eight patients with arrhythmia improved. On echocardiography, pulmonary regurgitation decreased in all patients. Right ventricular dilatation decreased in only 14 patients (52%). We conclude that pulmonary regurgitation after transannular patching can be treated with implantation of a cryopreserved pulmonary homograft with acceptable mortality and low morbidity. Clinical improvement results from reduction of the right ventricular volume overload rather than from decline in right ventricular dilatation. Arrhythmia as the only indication for operation is controversial.

Adolescent↗
PubMed1998

Arrhythmias in patients with mechanical ventricular dysfunction and myocardial stretch: role of mechano-electric feedback.

Patients with dilated cardiomyopathy, ventricular volume or pressure overload, or dysynergistic ventricular contraction and relaxation are prone to develop severe ventricular arrhythmias. In these patients it has been suggested that the abnormal mechanics of contraction can disturb 'mechano-electric feedback', also known as 'contraction-excitation feedback', which is defined as the development of electrophysiological changes during or after changes in mechanical loading. This electrical instability, expressed by significant changes in ventricular repolarization and refractoriness and by the development of afterdepolarizations, has been variously reported in isolated tissues and isolated ventricles as well as in hearts in vivo. Furthermore, it is known that many patients with supraventricular tachycardia but otherwise structurally normal hearts can develop atrial fibrillation and that atrial arrhythmias frequently occur in the setting of acute or chronic increases in atrial size and pressure. It is possible that changes in atrial load directly alter the electrophysiological properties of the atrium by an analogue mechanism of contraction-excitation feedback. This paper reviews the literature concerning mechanoelectric feedback involvement in rhythm disorders, with the aim of investigating, through basic and clinical research, the clinical and therapeutic implications.

Arrhythmogenic Right Ventricular Dysplasia↗
PubMed1992

Right ventricular wall motion disturbance and determinants of the appearance of hemodynamic right ventricular infarction.

In order to elucidate the mechanisms of the appearance of hemodynamic right ventricular infarction (RVI), we studied right and left ventriculograms and hemodynamic findings in 52 patients with acute inferior myocardial infarction. Right ventricular wall motion disturbance (RVWMD) was detected in 69% of patient but hemodynamic RVI was observed only in 16%. Among patients with RVWMD, there was no significant difference in right ventricular ejection fraction between those with (group III) and without (group II) hemodynamic RVI, suggesting that right ventricular (RV) systolic dysfunction does not independently produce hemodynamic RVI. Right ventricular end-diastolic volume index was similar in groups II and III in spite of higher mRA in group III. The result suggested that the RV compliance of group III was decreased. Heart rate (HR) was significantly lower in group III than in group II. Not only physiologic pacing but also VVI pacing significantly improved hemodynamics in patients with hemodynamic RVI. A positive correlation between HR and cardiac index was observed (r = 0.56, p < 0.001) in patients with RVWMD. Decreased RV compliance and bradycardia were considered to be determinants of the appearance of hemodynamic RVI. Volume loading did not improve hemodynamics significantly in patients with hemodynamic RVI.

Angiography, Digital Subtraction↗
PubMed2000

Right ventricular pressure and dilation during pressure overload determine dysfunction after pressure overload.

Volume expansion and inotropic stimulation are used clinically to augment cardiac output during acute right ventricular (RV) pressure overload. We previously showed that a brief period of RV pressure overload causes RV free wall dysfunction that persists after normal loading conditions have been restored. However, the impact of volume expansion and inotropic stimulation on the severity of RV dysfunction after acute pressure overload is unknown. We hypothesized that the severity of RV dysfunction after RV pressure overload would be related to the level of RV free wall systolic stress during RV pressure overload, rather than to the specific interventions used to augment RV function. Chloralose-anesthetized, open-chest pigs were subjected to 1 h of RV pressure overload caused by pulmonary artery constriction, followed by 1 h of recovery after release of pulmonary artery constriction. A wide range of RV free wall systolic stress during RV pressure overload was achieved by either closing or opening the pericardium (to simulate volume expansion) and by administering or not administering dobutamine. The severity of RV free wall dysfunction 1 h after RV pressure overload was strongly and directly correlated with the values of two hemodynamic variables during RV pressure overload: RV free wall area at peak RV systolic pressure (determined by sonomicrometry) and peak RV systolic pressure, two of the major determinants of peak RV free wall systolic stress. Opening or closing the pericardium, and using or not using dobutamine during RV pressure overload, had no independent effects on the severity of RV dysfunction. The findings suggest that the goal of therapeutic intervention during RV pressure overload should be to achieve the required augmentation of cardiac output with the smallest possible increase in RV free wall systolic stress.

Animals↗
PubMedDate not supplied

Right ventricular impairment in patients with chronic respiratory failure on home oxygen therapy--non-invasive assessment using a new Doppler index.

We evaluated the usefulness of the newly defined Doppler index combining systolic and diastolic myocardial performance, in assessing right-heart dysfunction in 29 patients with chronic respiratory failure caused by old tuberculosis who were on 24-h home oxygen therapy. We measured tricuspid inflow velocity, right-ventricular outflow velocity, late/early diastolic peak velocities (A/E), the ratio between pre-ejection period and ejection time (PEP/ET), and the new index of systolic and diastolic myocardial performance (SDMP) calculated as (isovolumetric contraction time + isovolumetric relaxation time)/ejection time. The calculated A/E, PEP/ET and SDMP in our patients were significantly higher than those in age-matched healthy subjects (n = 37, mean age 67 +/- 8 years). There was no overlap in the SDMP index between healthy subjects and patients and the index was not influenced by heart rate. Our results suggest that SDMP index is a better marker than A/E and PEP/ET for the assessment of right-ventricular impairment.

Aged↗
PubMed2000

Balloon pulmonary valvuloplasty in carcinoid syndrome.

Half of all patients with carcinoid syndrome develop cardiac involvement. Patients who have cardiac involvement have a significantly worse prognosis than those without, and death can occur directly as a result of cardiac involvement. A case of carcinoid syndrome in a 38 year old woman with lesions in the liver, who presented with right sided valvar abnormalities, a dilated right ventricle, and right ventricular pressure overload, is presented. In order to palliate the patient's symptoms and to decrease right sided pressures before major abdominal surgery, balloon pulmonary valvuloplasty was performed at the time of cardiac catheterisation. This resulted in a reduction in the pulmonary gradient and right ventricular pressure. Following the procedure, the patient's symptoms were completely relieved. She went on to laparotomy where the lesions in the liver were excised without complication.

Adult↗
PubMed1981

Effect of digoxin on right ventricular function in severe chronic airflow obstruction. A controlled clinical trial.

The effect of digoxin on the right and left ventricular ejection fractions in 15 patients with pulmonary heart disease caused by severe chronic airflow obstruction was studied in a double-blind, randomized, placebo-controlled trial. All patients were ambulatory and had clinical features of right but not left ventricular dysfunction. Equilibrium radionuclide angiography showed reduced right ventricular ejection fraction in all patients and reduced left ventricular ejection fraction in four. After 8 weeks of digoxin treatment, the abnormal left ventricular ejection fractions were normal; right ventricular ejection fractions increased only in those patients who had had abnormal left ventricular ejection fractions. We conclude that in patients with pulmonary heart disease, the right ventricular ejection fraction is abnormal and improves with digoxin treatment only when the left ventricular ejection fraction also is initially abnormal.

Aged↗
PubMed1995

Acute right ventricular failure, pathophysiology and treatment.

Right ventricular (RV) failure is now accepted as a pathophysiological entity. This acceptance has stemmed from the increasing facility of bedside assessment of pump function using thermodilution techniques. The subsequent improvement in the assessment of RV volume changes has allowed existing theories to be confirmed. The anatomical disposition and geometry of the right ventricle allow it to adapt very well to wide variations in preload, but poorly to increases in afterload. In the presence of increased afterload, RV stroke volume decreases linearly with increasing resistance and the ventricle eventually dilates. This dilation is then responsible for further RV failure, due to decreased right coronary artery flow (from systolo-diastolic to diastolic only) at a time when myocardial oxygen consumption is increased. Furthermore, RV dilation shifts the interventricular septum to the left, decreasing left ventricular preload and, hence, the cardiac output. An often lethal vicious circle is induced. The main therapeutic goals aimed at breaking this circle are restoration of adequate oxygen delivery to the myocardium and diminution of RV afterload.

Acute Disease↗
PubMed2005

Right ventricular failure after left ventricular assist device implantation: the need for an implantable right ventricular assist device.

Right ventricular failure after implantation of a left ventricular assist device is an unremitting problem. Consideration of portal circulation is important for reversing liver dysfunction and preventing multiple organ failure after left ventricular assist device implantation. To achieve these objectives, it is imperative to maintain the central venous pressure as low as possible. A more positive application of right ventricular assistance is recommended. Implantable pulsatile left ventricular assist devices cannot be used as a right ventricular assist device because of their structure and device size. To improve future prospects, it is necessary to develop an implantable right ventricular assist device based on a rotary blood pump.

Assisted Circulation↗
PubMed2004

Chronic hypoxia induces nonreversible right ventricle dysfunction and dysplasia in rats.

The purpose of this study was to evaluate the reversibility of right ventricular (RV) remodelling after pulmonary artery hypertension (PAHT) secondary to 3 wk of hypobaric hypoxia. A group of 10 adult male Wistar rats were studied and were the following: control normoxic (C), after 3 wk of chronic hypoxia (CH), and after 3 wk of exposure to hypoxia followed by 3 wk of normoxia recovery (N-RE). Mean pulmonary artery pressure was 11 +/- 2 mmHg in the C group, 35 +/- 2 mmHg in the CH group, and 14 +/- 3 mmHg in the N-RE group. RV function was assessed by echocardiography. In the CH group, the pulmonary flow measured in Doppler mode depicted a midsystolic notch and a decrease of the pulmonary acceleration time compared with control [17 +/- 1 vs. 34 +/- 1 ms (n = 10), respectively; P < 0.05]. RV thickening measured in M-mode was apparent in the CH group compared with the control group [2.84 +/- 0.40 vs. 1.73 +/- 0.26 mm (n = 10), P < 0.05]. In the N-RE group, the RV wall was significantly thinner compared with the CH group [1.56 +/- 0.08 vs. 1.73 +/- 0.26 mm (n = 10), P < 0.05]. The calculated RV diameter shortness fraction was not different between the CH group and C group (34 +/- 4.2% vs. 36 +/- 2.8%) but decreased in the N-RE group [20 +/- 2.4% (n = 10), P < 0.01]. The E-to-A wave ratio on the tricuspid Doppler inflow was significantly lower in the CH group and N-RE group compared with the C group [0.70 +/- 0.8 and 0.72 +/- 0.1 vs. 0.88 +/- 0.2 (n = 10), respectively; P < 0.05]. In the isolated perfused heart using the Langendorff method, RV compliance was increased in the CH group and decreased in the N-RE group. In the N-RE group, fibrous bands with metaplasia were observed on histological sections of the RV free wall. We conclude that PAHT induces nonreversible RV dysfunction with dysplasia.

Animals↗