Small left ventricles and biventricular repairs.
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OBJECTIVE: We sought to study the evolution of biventricular filling properties after coronary artery bypass grafting. BACKGROUND: The evolution of diastolic function as defined with newer echocardiographic modalities after coronary artery bypass grafting surgery is unknown in patients with preoperative left ventricular diastolic dysfunction. METHODS: Transthoracic echocardiography was performed preoperatively and 48 hours and 6 months after coronary artery bypass grafting in 49 patients (randomized to milrinone [n = 25]) or placebo [n = 24]) with preoperative left ventricular diastolic dysfunction classified according to published criteria. Mild right ventricular diastolic dysfunction was defined as the ratio of early to atrial filling velocity of less than 1 in transtricuspid flow or the velocity of reversed atrial flow of greater than 50% of that of systolic flow in hepatic venous flow or the ratio of tricuspid annulus velocity during early and atrial filling of less than 1 if both the ratio of early to atrial filling velocity and the ratio of systolic to diastolic velocity was greater than 1 in hepatic venous flow. Moderate right ventricular diastolic dysfunction was diagnosed when there was a ratio of early to atrial filling velocity of greater than 1 with a ratio of systolic to diastolic velocity of less than 1. Severe right ventricular diastolic dysfunction was defined as a ratio of early to atrial filling velocity of greater than 1 associated with reversed systolic wave in hepatic venous flow. RESULTS: Moderate and severe left ventricular diastolic dysfunction increased from preoperatively to 48 hours after coronary artery bypass grafting from 8.2% to 53.7% and from 2.0% to 9.7%, respectively (P < .0001, 48 hours vs preoperatively for both), and the patterns at 6 months were similar to those observed preoperatively. Similar evolution over time was found for right ventricular diastolic dysfunction. CONCLUSIONS: In patients with preoperative left ventricular diastolic dysfunction, biventricular filling patterns are impaired initially but return to preoperative status 6 months after coronary artery bypass grafting.
Arrhythmogenic right ventricular dysplasia is considered to be a slowly progressive disease in which left ventricular dysfunction and congestive heart failure usually appear at the end stage. The initial clinical presentation of this 56-year-old Japanese woman was left-sided heart failure, and the diagnosis was dilated cardiomyopathy, but her left ventricular size and ejection fraction regressed during 10 years of treatment, whereas her right ventricular parameters showed no change.
To evaluate the relationship between right and left ventricular function in patients with obstructive lund disease, we studied 10 normal subjects (group 1) and 37 patients with chronic obstructive pulmonary disease by first pass radionuclide angiography. These 37 patients were divided into three groups: nine with mild chronic obstructive pulmonary disease (group 2), 20 with severe chronic obstructive pulmonary disease (group 3) and eight with severe chronic obstructive pulmonary disease and primary left ventricular disease (group 4). In each subject right ventricular ejection fraction (RVEF), left ventricular ejection fraction (LVEF) and ejection fraction during first third of systole (first third LVEF) were calculated. (For table: see text.) p less than 0.05 versus 1. All subjects in group 2 had normal left ventricular and right ventricular function. In group 3, 11 of 10 (55 per cent) had a low RVEF and three of 20 (15 per cent) a low LVEF. However eight of 20 in this group (40 per cent) had a depressed first-third LVEF. The correlation between decline in RVEF and first-third LVEF was good r = 0.73. We conclude that (1) certain indices of early systolic left ventricular ejection are abnormal in many patients with chronic obstructive pulmonary disease and correlate with the decline in right ventricular function; (2) this is not seen in patients with mild chronic obstructive pulmonary disease and is worse in patients with underlying left-sided heart disease.
BACKGROUND: Thyroid gland dysfunction affects the structure and function of the heart. Tissue Doppler echocardiography is a new technique, and it has been used frequently in the evaluation of ventricular function. In the present study, right ventricular function was assessed in patients with overt or subclinical hypothyroidism and hyperthyroidism and in healthy subjects using the tissue Doppler method, and results were compared. PATIENTS AND METHODS: 20 healthy subjects and 63 patients diagnosed with overt and subclinical hypothyroidism and hyperthyroidism were included in the study. Annular and myocardial systolic peak velocities, early and late diastolic peak velocities, precontraction, total contraction and relaxation times of the right ventricle were recorded by tissue Doppler echocardiography. The results of the patients were compared to those of the controls. RESULTS: Myocardial systolic velocity was significantly higher in patients with hyperthyroidism. Annular and myocardial late diastolic velocities were found to be significantly lower in patients with overt hypothyroidism. Annular precontraction time was increased in patients with overt and subclinical hypothyroidism. Myocardial precontraction time was decreased in patients with hyperthyroidism, and increased in patients with overt hypothyroidism patients. Annular relaxation time was increased in patients with overt hypothyroidism. CONCLUSIONS: Right ventricular function is affected in patients with thyroid diseases. The tissue Doppler technique is a suitable tool to detect impairments in right ventricular function. There is a significant correlation between serum thyroid hormone levels and right ventricular velocities and time intervals.
OBJECTIVES: The goal of this study was to determine whether right ventricular (RV) ischemia is a contributory factor in the development of RV dysfunction in patients with primary pulmonary hypertension (PPH). BACKGROUND: Patients with advanced PPH develop RV dysfunction, characterized by a decreased cardiac output, increased right atrial pressure (RAP) and/or elevated RV end-diastolic pressure, which progresses to heart failure and death. The cause of this dysfunction is unknown. Right ventricular ischemia may play a role in its development. METHODS: From 1992 to 1999, a prospective study involving 23 patients with PPH at the Instituto Nacional de Cardiologia "Ignacio Chavez" (Mexico City, Mexico) was undertaken. These patients were evaluated clinically and further studied by echocardiography, right heart catheterization and stress myocardial scintigraphy using technetium 99m sestamibi. RESULTS: Nine patients of 23 were found to have scintigraphic images consistent with RV ischemia. Significant correlation was found between RV ischemia obtained through myocardial perfusion scintigraphy and elevation of RV end-diastolic pressure (p < 0.001), elevation of RAP (p < 0.037) and a decrease in mixed venous oxygen saturation (p < 0.0001). No other clinical or hemodynamic variables showed a significant correlation with RV ischemia. CONCLUSIONS: A direct correlation exists between RV ischemia, as determined by myocardial scintigraphy, and hemodynamic alterations suggestive of RV dysfunction in patients with PPH.
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BACKGROUND: Some of the most frequent manifestations of heart involvement in human immunodeficiency virus (HIV) infection include right and left ventricular dysfunction. The pathogenesis remains obscure. METHODS AND RESULTS: This prospective clinical and echocardiographic study involved 181 patients at all stages of HIV infection. We tested a set of clinical variables using a backward logistic regression model to assess their ability to independently predict the presence of ventricular dysfunction. The presence of pulmonary infections (all etiologies mixed) was the only variable independently associated with isolated right ventricular dysfunction (odds ratio = 4.08; P = .02). Signs suggestive of pulmonary arterial hypertension were present in 71% of the patients with right ventricular dilation. History of previous opportunistic infections (all etiologies mixed) (odds ratio = 10.9; P = .0026) and time since the diagnosis of acquired immunodeficiency syndrome more than 12 months (odds ratio = 6.6; P = .03) were the only two independent predictors of left ventricular dysfunction. CONCLUSIONS: Isolated right ventricular dysfunction may be secondary to pulmonary hypertension caused by repetitive pulmonary infections and not to primary myocardial disease. The aggressive treatment of opportunistic infections may become an important element of heart failure prophylaxis in HIV infection because they may be associated with left ventricular dysfunction.
OBJECTIVE: We evaluated the cardiovascular pathologic condition in the recipient twin in twin-to-twin transfusion syndrome and the influence of amnioreduction. STUDY DESIGN: Fetal echocardiograms and medical records of 54 pregnancies that were complicated by twin-to-twin transfusion syndrome were reviewed. Recipient twin right and left ventricular wall thickness, diameters, systolic and diastolic function, valve regurgitation, and structural cardiac defects were assessed at examination and after amnioreduction. RESULTS: At examination (n = 28 pregnancies), cardiomegaly because of right ventricular and/or left ventricular hypertrophy was observed in 58% of recipient twins, and biventricular hypertrophy was observed in 33% of recipient twins, without ventricular dilation. Biventricular diastolic dysfunction was present in two thirds of recipient twins, and right ventricular systolic dysfunction and significant atrioventricular valve regurgitation was observed in one third of recipient twins. Serial assessment (n = 21 pregnancies) revealed progressive biventricular hypertrophy and right ventricular systolic and biventricular diastolic dysfunction in most recipient twins. Steeper progression of hypertrophy, diastolic dysfunction, and structural or functional right ventricular outflow disease (20% incidence) were associated with an increased perinatal mortality rate. CONCLUSION: In twin-to-twin transfusion syndrome, the recipient twin has progressive biventricular hypertrophy with predominant right ventricular systolic and biventricular diastolic dysfunction. Despite amnioreduction, the cardiovascular disease persists and even progresses in many recipient twins.
BACKGROUND AND OBJECTIVES: Pericardial effusion (PE) is frequently found in patients infected with the human immunodeficiency virus (HIV), but its clinical significance remains unclear. Our purpose was to study the manifestations of HIV-infected patients with PE and the coexistence of these manifestations with other echocardiographic abnormalities, compared with patients without PE. METHODS: We reviewed 141 HIV-infected patients in whom echocardiographic study was performed. We studied their epidemiological, clinical, hematological, immunological, electrocardiographic (ECG) and echocardiographic characteristics and their in-hospital outcome. RESULTS: Patients with PE (n = 55), compared with those without PE (n = 86), were more often clinical stage C and immunological stage 3, had left-ventricular dysfunction and right-ventricular dilatation more frequently, and had been diagnosed as HIV-positive for a longer time. Seven patients with moderate to severe PE developed cardiac tamponade. Compared with patients with small PE (n = 34), those with moderate to large PE (n = 21), had pericardial rub, ECG repolarization abnormalities consistent with pericarditis, immunological stage 3, left-ventricular dysfunction and right-ventricular dilatation more frequently. In 3 patients, cardiac tamponade disappeared after anti-tuberculous therapy; in 3 cases, pericardial drainage was performed (anti-tuberculous therapy was not attempted); 1 patient with cardiac tamponade was not drainaged because he was a terminal patient with an extensive lymphoma. CONCLUSIONS: PE in HIV-infected patients is associated with (1) advanced stages of infection, and (2) left-ventricular dysfunction and right-ventricular dilatation; (3) presence of pericardial rub and ECG alterations consistent with pericarditis suggests the existence of moderate to large PE.
Acute right coronary artery occlusion proximal to the right ventricular (RV) branches results in right ventricular free wall dysfunction, exerting mechanically disadvantageous effects on biventricular performance. Depressed RV systolic function decreases transpulmonary delivery of left ventricular (LV) preload, resulting in diminished cardiac output. The ischemic right ventricle is stiff, dilated, and volume dependent, resulting in pandiastolic RV dysfunction and septally mediated alterations in LV compliance, which are exacerbated by elevated intrapericardial pressure. Under these conditions, RV pressure generation and output are dependent on LV-septal contractile contributions, governed by both primary septal contraction and paradoxical septal motion. When the culprit coronary lesion is distal to the right atrial (RA) branches, augmented RA contractility enhances RV performance and optimizes cardiac output. Conversely, more proximal occlusions result in ischemic depression of RA contractility, which impairs RV filling and performance, resulting in more severe hemodynamic compromise. Bradyarrhythmias limit output generated by the rate-dependent noncompliant ventricles. Hemodynamic compromise may respond to volume resuscitation and restoration of physiologic rhythm. Vasodilators and diuretics should generally be avoided. In some patients, parenteral inotropic stimulation may be required. The right ventricle appears to be relatively resistant to infarction and recovers even after prolonged occlusion. The term RV "infarction" appears to be somewhat of a misnomer, for in most patients acute RV dysfunction represents ischemic but predominantly viable myocardium. Although RV performance improves spontaneously even in the absence of reperfusion, recovery of function may be slow and associated with high in-hospital mortality. Reperfusion enhances recovery of RV performance and improves the clinical course and survival.
The paper deals with the development of a diagnostic and therapeutic algorithm of intraoperative heart failure during cardiosurgical operations on the basis of evaluation of systolic and diastolic functions of the left and right ventricles. The study included 101 patients with low cardiac output in the postperfusion period. All the patients suffered from coronary heart disease and they underwent myocardial revascularizing operations under extracorporeal circulation. In all the patients, in addition to traditional hemodynamic parameters (heart rate, blood pressure, central venous pressure), the functional status of the left and right ventricles was evaluated by transesophageal Doppler echocardiography (TED echoCG) and the thermodilution technique using a Swan-Ganz catheter having a prompt thermistor. Evaluating the diastolic and diastolic functions of the right and left ventricles makes it possible to identify 2 types of left and right ventricular failure: 1) that due to systolic dysfunction and 2) that due to concomitance of systolic and diastolic dysfunctions. Dobutrex (5-7.5 microg/kg/min) should be used in right ventricular systolic dysfunction. Amrinone (5-10 microg/kg/min) should be given to patients with concomitance of systolic and diastolic dysfunction; in this situation, a combination of dobutrex and nitroglycerin (100-150 ng/kg/min) may be used. The drugs of choice in impaired left ventricular systolic function are epinephrine (30-100 ng/kg/min), dopamine (5-10 microg/kg/min), or dobutrex (5-7.5 microg/kg/min). Their combination with sodium nitroprusside can enhance the efficiency of therapy. In patients with left ventricular failure caused by systolic and diastolic dysfunction, epinephrine, dopamine, or dobutrex may be combined with amrinone (5-10 microg/kg/min) or nitroglycerin (100-150 ng/kg/min).
AIM: Left ventricle impairment is very common in acromegaly. Concentric hypertrophy and diastolic dysfunction are observed at an early stage. Late left ventricle dilatation with systolic dysfunction may appear. Few reports have studied right ventricle diastolic function. METHODS: Twenty-seven acromegalic patients were included. Biventricular diastolic function was assessed using Doppler-echocardiography. Possible associations with hormonal activity, evolution time of illness, hypertension, left ventricular hypertrophy and systolic impairment on echocardiography were studied. RESULTS: Fifteen patients showed left ventricular diastolic dysfunction, whereas thirteen patients showed right ventricular diastolic dysfunction. A good correlation was observed between E/A relation of both ventricles (r = 0.70; p < 0.01) and isovolumetric relaxation time (r = -0.60; p < 0.01). The right ventricular E/A relation correlated with left ventricular mass index and significance was almost achieved with the presence of hypertension. There was no statistical correlations between the right ventricular E/A relation and hormone values or evolution time of illness. The left ventricular E/A relation showed a significant association with left ventricular mass index, isovolumetric time index and evolution time of illness. There were no statistical association with hormone values. CONCLUSIONS: The high prevalence of right ventricular diastolic dysfunction observed in acromegaly suggests the presence of acromegalic myocardiopathy.
The goal of this study was to evaluate the role of Doppler time interval-derived myocardial performance index (MPI) in the setting of acute right ventricular myocardial infarction (RVMI). Inferior myocardial infarction is accompanied by RVMI in over a third of cases. We do not have easily applicable noninvasive tools for reliably quantifying the right ventricular (RV) dysfunction in RVMI and to serially follow alterations. Clinical and echocardiography data of all acute inferior myocardial infarction (IMI) admissions (n = 135) to our referral teaching institute were prospectively collected for the study. After exclusions, study group comprised of 36 patients with RVMI diagnosed by >/=1 mm ST segment elevation in V3R-V5R of right-sided ECG and 63 patients without RVMI constituted the control group. All patients underwent echocardiography within 24 hours of admission. Normal range of MPI for our laboratory was estimated from 50 age-matched healthy subjects. RV MPI was elevated to a mean of 0.53 +/- 0.22 in RVMI (Normal MPI 0.20 +/- 0.05, P-value < 0.001). IMI without RVMI did not elevate MPI significantly (0.21 +/- 0.17, P-value NS). Repeat MPI estimation in 11 RVMI (7 thrombolyzed) patients after 5 days showed dramatic reduction (0.23 +/- 0.12, P-value < 0.001). This reduction was noted irrespective of thrombolysis. RV MPI >/= 0.30 has high sensitivity (82%) and specificity (95%) for the diagnosis of RVMI in the presence of acute IMI. MPI can reliably diagnose RV infarction. It can be used to quantify right ventricular dysfunction and assess acute improvements in RV function.
Acute proximal right coronary artery (RCA) occlusion results in profound right ventricular (RV) ischemic dysfunction; however, chronic RV dysfunction at rest from persistent RCA occlusion is rare. We studied the responses of the right ventricle to exercise in patients with chronic proximal RCA occlusion, demonstrating preserved RV free wall motion and appropriate augmentation of ejection fraction in nearly all cases.
OBJECTIVES: Early morbidity and mortality post cardiac transplantation is frequently caused by right ventricular failure; this is usually attributed to an elevated pulmonary vascular resistance in the recipient. Brain death in the donor is recognised as causing left ventricular dysfunction, but its effects on the right ventricle have not previously been studied. The aim of this study was to investigate right ventricular function following brain death, using a canine model. METHODS: The hearts of 33 dogs were instrumented with micromanometers, flow probes and dimension transducers to measure minor/major axes, and right and left ventricular free wall to septal distances. Left ventricular volume was calculated according to the prolate ellipsoid model and right ventricular volume was calculated according to the shell subtraction method. Systolic function for left and right ventricles was analysed by plotting ventricular stroke work vs. end-diastolic volume during a caval occlusion (preload-independent recruitable stroke work PRSW). Brain death was instigated by inflation of a subdurally placed intracranial balloon; subsequently blood pressure was maintained with intravenous fluid whilst no inotropic medications were given. Data were collected at baseline, and at 2 and 4 h thereafter. A two-tailed paired Student's t-test was applied to compare post-brain death data with baseline measurements. RESULTS: All animals had an initial hyperdynamic response post brain death ensued by the development of diabetes insipidus. Brain stem death was validated by neuropathological examination at the termination of the experiments. Right and left ventricular systolic function had deteriorated significantly 2 h post brain death by 34.4% (+/- 5.1%, P < 0.001) and 20.4% (+/- 3.4%, P < 0.001), respectively, from baseline PRSW [RV = 23.6 erg.10(3) (+/- 1.5), LV = 76.2 erg.10(3) (+/- 3.5)]. This deterioration remained at 4 h post brain death (29.4% (+/- 4.9%, P < 0.001) and 21.2% (+/- 4.3%, P < 0.001), respectively). (The results are expressed as mean and S.E.M.). CONCLUSIONS: Brain death causes a significant decrease in left and right ventricular function. The injury to the right ventricle is more prominent than the left ventricle, and at 2 h post brain death it is significantly greater. Failure of the right ventricle post transplantation in clinical practice may be related to this brain death induced injury. Further studies are required to investigate the mechanisms of this injury.
Eighty-five consecutive patients with idiopathic dilated cardiomyopathy were categorized according to the presence (biventricular dysfunction) or absence (left ventricular [LV] dysfunction) of reduced right ventricular ejection fraction (<35%) along with reduced LV ejection fraction (<50%). Compared with the 36 patients with LV dysfunction, the 49 patients with biventricular dysfunction had significantly worse New York Heart Association functional class (2.7+/-0.6 vs 1.9+/-0.5; p <0.001), LV ejection fraction (26+/-10% vs 34+/-8%; p <0.0001), and outcome (transplant-free survival, 55% vs 89%; p <0.001). Thus, dilated cardiomyopathy is frequently characterized by biventricular involvement, which identifies a more severe disease and a worse long-term prognosis.
OBJECTIVE: The purpose of this study was to examine and compare the systemic and pulmonary hemodynamic effects of a central venous infusion of adenosine in cardiac surgical patients. DESIGN: Prospective; each subject served as his/her own control. SETTING: University Hospital and Veteran's Affairs Medical Center. PATIENTS: Ten cardiac surgical patients (age 56 +/- 6 years) were studied in the operating room under general anesthesia after weaning from cardiopulmonary bypass. Pulmonary vascular resistance (PVR), systemic vascular resistance (SVR), mean pulmonary arterial pressure (MPAP), and mean systemic arterial pressure (MAP) were determined before, during, and after central venous infusion of adenosine (50 micrograms/kg/min) for 15 min. Statistical analysis was by analysis of variance; significance was accepted at p < 0.05. RESULTS: Adenosine produced selective vasodilation of the pulmonary vascular bed: both PVR and MPAP were significantly reduced during adenosine infusion without changes in either SVR or MAP. PVR and MPAP returned to preinfusion levels after cessation of the infusion. Adenosine effectively reduced PVR and pulmonary arterial pressure without decreasing SVR or systemic arterial pressure. CONCLUSIONS: Adenosine may be used clinically as a selective pulmonary vasodilator to optimize pulmonary hemodynamics without adverse systemic hemodynamic effects in cardiac surgical patients. It may be particularly valuable in patients with right heart dysfunction by selectively lowering right ventricular afterload.