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At least 649 records · Page 36Linked to original sources
PubMed2005

Mechanisms of oxygen demand/supply balance in the right ventricle.

Few studies have investigated factors responsible for the O2 demand/supply balance in the right ventricle. Resting right coronary blood flow is lower than left coronary blood flow, which is consistent with the lesser work of the right ventricle. Because right and left coronary artery perfusion pressures are identical, right coronary conductance is less than left coronary conductance, but the signal relating this conductance to the lower right ventricular O2 demand has not been defined. At rest, the left ventricle extracts approximately 75% of the O2 delivered by coronary blood flow, whereas right ventricular O2 extraction is only ~50%. As a result, resting right coronary venous PO2 is approximately 30 mm Hg, whereas left coronary venous PO2 is approximately 20 mm Hg. Right coronary conductance does not sufficiently restrict flow to force the right ventricle to extract the same percentage of O2 as the left ventricle. Endogenous nitric oxide impacts the right ventricular O2 demand/supply balance by increasing the right coronary blood flow at rest and during acute pulmonary hypertension, systemic hypoxia, norepinephrine infusion, and coronary hypoperfusion. The substantial right ventricular O2 extraction reserve is used preferentially during exercise-induced increases in right ventricular myocardial O2 consumption. An augmented, sympathetic-mediated vasoconstrictor tone blunts metabolically mediated dilator mechanisms during exercise and forces the right ventricle to mobilize its O2 extraction reserve, but this tone does not limit resting right coronary flow. During exercise, right coronary vasodilation does not occur until right coronary venous PO2 decreases to approximately 20 mm Hg. The mechanism responsible for right coronary vasodilation at low PO2 has not been delineated. In the poorly autoregulating right coronary circulation, reduced coronary pressure unloads the coronary hydraulic skeleton and reduces right ventricular systolic stiffness. Thus, normal right ventricular external work and O2 demand/supply balance can be maintained during moderate coronary hypoperfusion.

Animals↗
PubMed2006

[Study of the echocardiographic diagnosis of acute pulmonary thromboembolism and risk factors for venous thromboembolism].

OBJECTIVES: To identify the relationship of risk factors for atherosclerosis with venous thromboembolism (VTE) and the utility of transthoracic echocardiography in acute pulmonary thromboembolism (APTE). METHODS: In 75 patients with VTE (VTE group), 101 patients with suspected VTE (N group), and 50 control subjects (control group), the frequency of atherosclerosis risk factors such as hyperlipidemia, obesity, hypertension, smoking, and diabetes mellitus and the number of risk factors were evaluated. Transthoracic echocardiographic findings such as tricuspid regurgitation, right ventricular dilation, pulmonary hypertension, and right ventricular dysfunction were evaluated in 15 patients with APTE (APTE group) and 38 patients in the N group (NC group). RESULTS: The incidence of hyperlipidemia in the VTE group was statistically higher than that in the control group (odds ratio 2.16, 95% confidence interval 1.43-3.08). Additionally, the incidence of obesity was higher in the VTE and N groups than in the control group (odds ratio was 2.76, 95% confidence interval 1.67-4.37). Risk factors other than obesity and hyperlipidemia and the number of risk factors were not significant. The incidence of tricuspid regurgitation, right ventricular dilation, and pulmonary hypertension in APTE was statistically greater than that in NC group. Right ventricular dilation and right ventricular dilation + tricuspid regurgitation are reliable findings in echocardiography. However, even combining with tricuspid regurgitation, right ventricular dilation is insufficient to identify or screen patients with APTE. CONCLUSIONS: Hyperlipidemia and obesity may be risk factors for VTE. However, obese patients can manifest similar findings to VTE. Although transthoracic echocardiograpghy is not recommended as a diagnostic or screening test in APTE, it should be used as an ancillary test.

Acute Disease↗
PubMed1990

Atrial natriuretic factor in patients with right ventricular infarction.

To determine the possible role of atrial natriuretic factor in right ventricular infarction, serial measurements of this hormone were performed in 21 patients with acute inferior myocardial infarction. All patients underwent enzymatic, electrocardiographic, echocardiographic and coronary arteriographic studies. Ten patients also had right heart hemodynamic measurements. Eight patients had evidence of an associated right ventricular infarction (Group I) and 13 patients did not (Group II). Enzymatically estimated infarct size, presence of left heart failure and arrhythmias were similar in both groups. Mean arterial pressure in Group I (72.1 +/- 4.4 mm Hg) was significantly lower (p = 0.02) than in Group II (89.5 +/- 4.6 mm Hg). Seven (88%) of the eight patients in Group I had elevated right atrial pressures and a higher incidence than Group II of prolonged hypotension (75%) and right ventricular dysfunction (75%) clinically and by echocardiography. Plasma atrial natriuretic factor levels (mean values +/- SEM in pg/ml) for days 1, 2, 3 and 7 after infarction were, respectively: 152 +/- 30, 165 +/- 48, 199 +/- 27 and 189 +/- 31 for Group I versus 55 +/- 9, 55 +/- 11, 61 +/- 13 and 77 +/- 20 for Group II. The difference between groups was significant for days 1 (p less than 0.05), 3 and 7 (p less than 0.01) and not significant for day 2 (p = 0.07). These findings show that atrial natriuretic factor elevation is part of the neurohumoral response to right ventricular infarction and are consistent with the hypothesis that atrial natriuretic factor may play a pathophysiologic role in the right ventricular infarct syndrome.

Adult↗
PubMed1995

The forgotten chamber: the importance of the right ventricle.

Historically, the right heart was viewed as less important than the left heart in the maintenance of normal overall hemodynamic performance. However, there is now considerable evidence that emphasizes the significance of intact right ventricular (RV) function. The RV's anatomy and physiology are reviewed in order to provide insight into how changes in volume can be accommodated within a low-pressure environment and how this contributes to hemodynamic stability. The interdependent relationship between the right and left ventricles is also explored. The contribution of RV performance to overall hemodynamics is best exemplified when the RV becomes diseased. RV infarction, atrial septal defect, and cor pulmonale are used as examples to illustrate the dramatic sequelae associated with RV dysfunction, as well as to identify the RV's specific adaptive mechanisms.

Heart Septal Defects, Atrial↗
PubMed2006

Arrhythmogenic right-ventricular dysplasia/cardiomyopathy.

PURPOSE OF REVIEW: Arrhythmogenic right-ventricular dysplasia is a rare inherited disease characterized by right-ventricular dysfunction and ventricular arrhythmias. The purpose of this article is to review recent developments concerning the diagnosis, genetics, and management of patients with this disease. RECENT FINDINGS: In the past few years important new information has emerged regarding the role of magnetic resonance imaging in the diagnosis of arrhythmogenic right-ventricular dysplasia. Although magnetic resonance imaging is a very sensitive tool, it is also the most common reason for over diagnosis of this condition. There have also been important new breakthroughs in the genetic basis of arrhythmogenic right-ventricular dysplasia; it now appears that most forms result from mutations in genes encoding desmosomal junction proteins. This may explain why arrhythmogenic right-ventricular dysplasia preferentially impacts the thin right ventricle. Other studies have demonstrated the important role of implantable cardioverter defibrillator therapy in the management of patients with arrhythmogenic right-ventricular dysplasia. In the USA, most patients who meet the Task Force criteria for the disease undergo placement of an implantable cardioverter defibrillator for prevention of sudden cardiac death. SUMMARY: Arrhythmogenic right-ventricular dysplasia is a rare disease. Recent new findings concerning the diagnosis and management of these patients should have direct implications regarding the evaluation and management of patients with this rare, but potentially life-threatening, disorder.

Anti-Arrhythmia Agents↗
PubMed1988

Current approach to treatment of primary pulmonary hypertension.

Based upon our experience with a cohort of 46 patients referred to the UCHSC from April, 1980 to April, 1987 for evaluation and treatment of PPH, we currently assess acute pulmonary vasoreactivity as defined by the patient's response to intravenous PGI2 during the initial diagnostic catheterization. A 3 to 5 day trial of high dose oral diltiazem treatment (720 mg/day maximum) is given while monitoring the patient in the clinical research center to detect significant side effects including arrhythmias, orthostatic systemic hypotension, arterial desaturation, and worsened right ventricular dysfunction. We believe it is necessary to recatheterize each patient to establish the efficacy of calcium antagonist treatment prior to discharge. Those patients who are responsive to diltiazem are discharged and followed in our pulmonary hypertension clinic. Since an occasional patient will deteriorate after several weeks of therapy, repeat right heart catheterization after 8 weeks of treatment is used to determine which patients should be continued on diltiazem for chronic therapy. Approximately 30 percent of our patients with PPH have been improved on diltiazem treatment. Most patients who have a good response to treatment after eight weeks continue to benefit from long-term treatment. It appears that the response to an acute infusion of PGI2 is useful in safely identifying those PPH patients who are likely to benefit from vasodilator therapy. Debilitated patients who are unresponsive to PGI2 and vasodilator therapy are considered potential candidates for cardiopulmonary transplantation.

Administration, Oral↗
PubMed2003

Echocardiographic assessment of right ventricular obstruction in hypertrophic cardiomyopathy.

Echocardiography was used to evaluate the incidence, flow dynamics and morphological characteristics of right ventricular obstruction in 91 patients with hypertrophic cardiomyopathy. Color flow mapping was used to define the sites of obstruction in the left and right ventricles. Ventricular obstruction was considered to be present if the flow velocity was less than 2.0 m/s as measured by continuous wave Doppler. The thickness of both the right ventricular free wall and anterior ventricular septum was measured to assess the magnitude and extent of hypertrophy. Right ventricular obstruction was present in 14 patients of whom 6 (43%) had left ventricular obstruction also. The right ventricular obstructions were found in the outflow tract (9 patients), mid-base septal bulge (2 patients) and apical trabecular region (3 patients). Doppler waveform was confined to systole in all patients with obstruction in the outflow tract and in one of the patients with mid-base septal bulge. Moreover, the flow wave persisted into early diastole in 4 patients, including 2 with apical trabecular obstruction. The thickness of both the right ventricular free wall and anterior ventricular septum suggested that these hypertrophied regions were the sites of right ventricular obstruction. Thus, echocardiography was useful in evaluating right ventricular obstruction in hypertrophic cardiomyopathy.

Adult↗
PubMed1983

[The value of temporary electrosystolic pacing for treating low output in posterior necrosis with adiastole].

Early catheterisation was performed in 27 patients with an acute inferior myocardial infarction less than 3 days old complicated by signs of low output with right ventricular dysfunction. All patients had hemodynamic criteria of adiastole (PCP = 14.9 +/- 31 mmHg and LVEDP = 14.1 +/- 4.7 mmHg) with low cardiac output (CI = 1.41 +/- 0.32 l/min/m2). An atropine resistant bradycardia was characteristic (HR = 65 +/- 17.2/min) due to advanced or complete AV block (11 cases), sinoatrial block (3 cases, one with right atrial standstill) or sinus/parasinus rhythm (13 cases) inappropriate to the severity of their hemodynamic state. Although the prognosis based on the discriminating linear function FI = -0.427 + 0.00121 LVW - 0.00125 TPR was initially poor and predicted the death of 21 out of the 27 patients at one month, the outcome was usually favourable and only 8 patients died during the first month. Fifteen patients were treated by temporary endocavitary RV pacing. As the heart rate was increased from 53.8 +/- 11.2 to 92.4 +/- 4.9/min, the CI rose from 1.35 +/- 0.26 to 1.85 +/- 0.46 l/min/m2 (p less than 0.001) with a fall in SI from 26.7 +/- 8.3 to 20.1 +/- 5.6 ml/beat/m2 (p less than 0.005). The results were even further improved in 3 cases by sequential A-V pacing. The observed hemodynamic improvement continued during the period of pacing providing volumic expansion maintained LVEDP above 10 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1998

[Valve diseases in the aged: when to operate?].

Valvular lesions, especially aortic stenosis, are not uncommon among the elderly, a sector of the population that is increasing in relative (extreme decrease in birth rates) and absolute terms (reduction of morbidity/mortality due to health and social advances), and their treatment presents a major challenge to the health system. Advanced age constitutes a surgical risk, but this is more likely due to a greater prevalence of comorbid conditions than to an intrinsic effect of old age. Moreover, the morbid effects of age are extremely variable, and an individualized evaluation of the problem is required. The decision to surgically intervene in an elderly patient must take into account of three aspects: a) that the valvular lesion has important hemodynamic consequences; b) that the symptoms are a product of the lesion and not of a concomitant disease, and c) that there is no comorbid condition whose symptoms and prognosis are even worse than the valvular disease itself. The psychological attitude of patients and their family members is also a factor to be considered. In severe aortic stenosis, valve substitution normally has a highly effective palliative effect, although at the cost of a moderately increased surgical risk. In mitral stenosis, preference should be given when possible to valvuloplasty with a balloon catheter. In degenerative mitral regurgitation, reconstructive techniques and prosthetic substitution with chordal preservation have considerably improved surgical outcomes, so that surgery is now indicated earlier to avoid the development of irrecoverable ventricular dysfunction. In mitral regurgitation of ischemic origin, structural damage (rupture of papillary muscle) must be differentiated from functional damage (dysfunction of papillary muscle); in the former, surgery is normally mandatory with a favorable outcome; in the latter the issue is more complex, and the possibility of improving the regurgitation by angioplasty of the culprit vessel must be thoroughly explored. The valvular sequelae of infectious endocarditis, a disease with higher incidence in old age, receive the same treatment at younger ages. Finally, in autochthonous tricuspid regurgitation, which can appear years after successful left side heart surgery, the decision to intervene is more difficult; in most cases it may be an expression of right ventricular dysfunction and a conservative approach would be indicated.

Age Factors↗
PubMed2001

Acute effects of pulmonary artery banding in sheep on right ventricle pressure-volume relations: relevance to the arterial switch operation.

The first stage of the two-stage arterial switch operation (ASO) for transposition of the great arteries (TGA) is associated with depressed ventricular function and an unstable immediate post-operative course. It is unclear if this is because of the acute increase in afterload of the thin-walled, low-pressure ventricle by pulmonary artery banding (PAB). To determine the acute effects of afterload increase on the contractile function of thin-walled ventricles, we studied the right ventricular pressure-volume relations of seven sheep before and 30 min after PAB using combined pressure-conductance catheters during inflow reduction. Load independent indices of systolic and diastolic performance were derived from these relations. Pulmonary artery banding increased the mean ratio between right and left ventricular systolic pressure from 0.34 +/- 0.05 to 0.64 +/- 0.10, P < 0.05 (mean +/- SD). There were no significant changes in heart rate and end-systolic volume after banding although there was an incremental trend in the end-diastolic volume and stroke volume. Right ventricular output (530 +/- 163-713 +/- 295 mL min (-1), P < 0.05), slope of the end-systolic pressure-volume relation (ESPVR) (3.7 +/- 2.8-10.0 +/- 4.8 mmHg mL (-1), P < 0.05) and slope of the pre-load recruitable stroke work (PRSW) relation (9.6 +/- 1.8-15.0 +/- 3.1 mmHg, P < 0.05) were significantly increased indicating improved contractile state after banding. The diastolic function curve was unchanged after banding although the right ventricle (RV) was operating at a larger end-diastolic volume. Hence, the RV of sheep responded to acute pressure overload by demonstrating enhanced contractility and evidence of the Frank-Starling mechanism without associated change in right ventricular diastolic performance.

Animals↗
PubMed1986

Severe right ventricular failure after Mustard or Senning operation. Two-stage repair: pulmonary artery banding and switch.

Since early 1981 I have been banding the pulmonary arteries of patients in whom severe right ventricular dysfunction has developed after atrial repair of transposition of the great arteries. The purpose of banding is to "retrain" the left ventricle. Of the four patients so treated, two developed adequate left ventricular pressures and have successfully undergone an arterial switch and takedown of the atrial repair. The early results are impressive. Right ventricular function has returned to normal in both patients and tricuspid valve regurgitation has resolved. In one patient moderate aortic valve regurgitation also appears to have largely resolved.

Blood Pressure↗
PubMedDate not supplied

[Permanent AV junction (Coumel type) reciprocal tachycardia].

UNLABELLED: Permanent auriculo-ventricular junctional reciprocating tachycardia is a special form of tachycardia usually incessant, secondary to an slow retrograde conduction pathway. OBJECTIVE: To establish the clinical, electrophysiological characteristics and therapy results in patients with this diagnosis. METHOD: Descriptive study. RESULTS: Nine patients with average age 28.1 +/- 19.2 years, six women. Seven patients presented with dyspnea or palpitations. The left ventricular ejection fraction before treatment was 43.3 +/- 19.5%. The electrocardiographic findings were: heart rate of 139.2 +/- 16.7 bpm, QRS 78.9 +/- 16.2 ms and RP'/P'R relation of 1.8 +/- 0.5. The location of the accessory pathways was: right postero-septal in seven (77.7%), left lateral in one (11.15%) and left postero-lateral in one (11.15%). Radiofrequency ablation was performed in eight patients with an 87.5% success rate, two cases were taken to surgery with successful treatment, one of them after percutaneous ablation failure. Those with systolic left ventricular dysfunction recover their function in the follow-up. Any case has recurred. CONCLUSIONS: In our center, permanent auriculo-ventricular junctional reciprocating tachycardia is an infrequent arrhythmia, predominantly in women and associated with reversible left ventricular dysfunction. Right postero-septal was the most frequent localization of the pathway. Radiofrequency ablation was performed successfully in 87.5% of cases.

Adolescent↗
PubMed2000

Morphology of right ventricular paced beats in posterior myocardial infarction.

Premature ventricular beats or paced beats can unmask new or old myocardial infarction when sinus beats fail to exhibit the typical infarct pattern. Knowledge of their morphology is vital, since they may be the earliest or even the only evidence of a myocardial infarction in certain cases. Morphology of premature ventricular beats or paced beats in anterior, anteroseptal, and inferior infarct has been described but not in the setting of a posterior infarct. We describe the morphology of right ventricular paced beats in a patient with posterior infarct and discuss its significance.

Aged↗
PubMed2005

Increased plasma levels of natriuretic peptide type B and A in children with congenital heart defects with left compared with right ventricular volume overload or pressure overload.

AIM: Natriuretic peptide levels B (BNP) and A (ANP) have been described in children with congenital heart defects (CHD) with pressure and volume overload. However, the impact of ventricular morphology per se on natriuretic peptide levels has not been reported. The aim of the present study was to evaluate plasma BNP and ANP in children with CHD with left or right ventricular volume or pressure overload. METHODS AND RESULTS: Plasma BNP and ANP were analysed in 61 children, median age 3.1 (0.3-16.2) years. Haemodynamic load was evaluated by echo-Doppler and/or catheterization measurements and classified as: pressure overload of the right (RV pressure) or left (LV pressure) ventricle, or volume overload of the right (RV volume) or left (LV volume) ventricle, of a sufficient degree to indicate surgery/catheter intervention. Twenty-three children, with a median age of 1.1 (0.1-8.3) years, without heart disease, served as controls for the natriuretic peptide measurements. Children in the LV volume group had significantly higher BNP and ANP values, 55.4 ng l-1 (10.7-352) and 164 (31.8-346), than children in the RV volume, 15.6 (0.0-105.1) and 57.2 (11.3-234.1), LV pressure, 6.8 (0.7-170) and 40.8 (12.6-210), and RV pressure, 18.0 (5.0-29.1) and 69.3 (8.7-182), groups respectively (P<0.0001). The values in the LV pressure group were close to the values in the Control group, 4.7 (0.0-17.7) and 32.9 (11.7-212.1), respectively (P=0.051 and P=0.378, respectively). CONCLUSIONS: Plasma concentrations of BNP and ANP were higher in children with CHD with left ventricular volume overload compared with right ventricular volume overload or pressure overload.

Adolescent↗
PubMed1993

Support of the perioperative failing heart with preexisting ventricular dysfunction: currently available options.

Perioperative support of the patient with preexisting biventricular failure requires simultaneous optimal manipulation of heart rate and rhythm, loading conditions, and contractility. Patients with preexisting ventricular dysfunction will have alterations in beta-adrenergic receptors, resulting in decreased responsiveness to catecholamines. Even patients with previously normal ventricular function can develop ventricular dysfunction caused by reperfusion injury and other potentially damaging effects of extracorporeal circulation. The mainstay of therapeutic agents used to allow separation from cardiopulmonary bypass are catecholamines, which stimulate alpha- and beta-adrenergic receptors. Submaximal responses to beta 1-adrenergic stimulation can occur in the down-regulated heart. The phosphodiesterase inhibitors provide both inotropic support and vasodilatation, which improves both systolic and diastolic function and bypasses beta-adrenergic receptors. When administered in combination, catecholamine and cyclic-AMP-specific phosphodiesterase inhibitors can have additive effects to restore beta 1-adrenergic responsiveness. Combination therapy provides an important therapeutic option to facilitate separation from cardiopulmonary bypass. Pharmacologic intervention for right ventricular dysfunction focuses on reversal of pulmonary vasoconstriction with nitrates, beta 2-adrenergic agents, phosphodiesterase inhibitors and prostaglandin E1.

Cardiac Output, Low↗
PubMed2004

Chronic upper airway obstruction and cardiac dysfunction: anatomy, pathophysiology and anesthetic implications.

The causes of obstruction to airflow in the pediatric upper airway include craniofacial disorders, subglottic stenosis, choanal atresia, syndromes associated with neuromuscular weakness, and the most common, hypertrophy of the tonsils and adenoids. Abnormal breathing can adversely affect craniofacial growth, and abnormal craniofacial development can promote upper airway obstruction. Chronic upper airway obstruction often presents with evidence of obstructive sleep apnea syndrome; in severe cases these children also present with pulmonary hypertension and cor pulmonale. The development of pulmonary hypertension and right heart dysfunction from chronic upper airway obstruction is complex. Hypoxemia and hypercarbia-induced respiratory acidosis are potent mediators of pulmonary vasoconstriction that can lead to reversible and irreversible chronic changes in the pulmonary vasculature. It is likely that production of various neurohumoral factors in response to hypoxemia and respiratory distress may further promote pulmonary hypertension, right ventricular dysfunction, and consequent impairment of systemic cardiac output. The anesthetic considerations for children undergoing adenotonsillectomy for chronic airway obstruction are significant. These children are at high risk for complications such as laryngospasm, desaturation, stimulation of pulmonary hypertension and cardiac dysfunction, pulmonary edema, postoperative upper airway obstruction, and respiratory arrest. Because of underlying condition(s) (facial abnormalities, neuromuscular disease, etc.), successful adenotonsillar surgery may not improve upper airway obstruction significantly, especially in the immediate postoperative period when edema, bleeding and the effects of anesthetics and analgesics are present.

Airway Obstruction↗