Cause Of Left Ventricular Failure Research Articles

Ultrasound patterns of pulmonary edema

Since its first description in 1967 (1), acute respiratory distress syndrome (ARDS) represents a well known major clinical problem in intensive care units (ICUs), carrying a high morbidity and mortality. Differentiating between hydrostatic or cardiogenic pulmonary edema (CPE) and ARDS is challenging, especially in the early stages of illness (2). This diagnostic task becomes more difficult in older patients, where a higher number of morbidities often coexists. Moreover, in septic patients with ARDS, the myocardium is dysfunctional due to systemic inflammatory activation and mitochondrial impairment, and sepsis related cardiomyopathy (3) is a recognized cause of left ventricular failure and of an increase in hydrostatic extravascular lung water and CPE.

Left Ventricular Noncompaction: A Rare Cause of Heart Failure in a HIV Patient

Background: Heart failure in patients with human immunodeficiency virus (HIV) is often from dilated cardiomyopathy as a result of HIV itself, drug myotoxicity, secondary infections, or druginduced atherosclerosis. Left ventricular noncompaction (LVNC) is a rare cardiac congenital abnormality which occurs due to early arrest of endomyocardial morphogenesis. Case: A 47- year-old female patient with HIV presented with sudden onset shortness of breath and symptoms of congestive heart failure. Echocardiography showed noncompacted endocardium with reduced left ventricular function. She was subsequently diagnosed with LVNC. Discussion: Multiple etiologies have been implicated in cardiomyopathy among HIV patients. LVNC is a rare cause of left ventricular failure, particularly in this population. Echocardiography plays a pivotal role in the diagnosis. Conclusion: It is often challenging to identify the underlying cause of cardiomyopathy in a patient with HIV. While LVNC is a rare cause of left ventricular failure, typical findings on echocardiography can obviate the need for a more complex evaluative strategy.

Neonatal Hemangiomatosis and Atrial Septal Defect: A Rare Cause of Right Heart Failure in Infancy

Neonatal hemangiomatosis is a well-recognized cause of left ventricular failure. We describe an infant with neonatal hemangiomatosis and an ostium secundum atrial septal defect who developed severe right heart failure. This was due to the combination of increased flow through the right heart as a result of the atrial septal defect, and the background high cardiac output from the massive arteriovenous shunting and multiple hemangiomas. In addition, the multiple hepatic hemangiomas may exert a vasoactive influence on the pulmonary vasculature.

Doppler echocardiographic evaluation of left ventricular diastolic function after surgical correction of atrial septal defect during childhood.

Transmitral flow was studied using Doppler echocardiography with the A/E ratio as a parameter of left ventricular diastolic function in 21 patients (ages 2.5-30.0 years) who had undergone early surgical correction of an isolated secundum type atrial septal defect (ASD) compared to a healthy cohort of 21 subjects. Pre- and postoperative M-mode recordings were compared in 12 of the 21 patients to evaluate the effect of operation on interventricular septal motion (IVS) and left ventricular (LV) and right ventricular (RV) end-diastolic diameter ratio (LVDD/RVDD) as parameters of right ventricular volume overload. No significant difference in A/E ratio was found between the patient and control groups. IVS was shown to normalize in 11 of 12 patients postoperatively and to improve from paradox to flattened in 1 of 12. LVDD/RVDD increased from 1.26 +/- 0.31 to 2.10 +/- 0.51 (p = 0.0008), with no significant difference remaining between the control and patient groups postoperatively. These findings support the conclusion that an intrinsic abnormality of the left ventricle is not responsible for its diastolic dysfunction in patients with ASD who develop left ventricular failure, thereby implicating an acquired abnormality. Mechanical sequelae of right ventricular volume overload were shown to normalize in all patients subsequent to operation in the present study, and therefore cannot be excluded as a cause of left ventricular failure in ASD.

Left ventricular distensibility and passive elastic stiffness in atrial septal defect

Diminished left ventricular distensibility has been postulated as a cause of left ventricular failure in atrial septal defect. To evaluate this hypothesis the indexes of left ventricular compliance and stiffness were estimated in 15 patients with atrial septal defect and the results compared with those in 10 normal subjects. Age, peak left ventricular systolic pressure, end-diastolic pressure, ejection fraction and cardiac index did not differ significantly between groups. Left ventricular end-diastolic volume for the atrial septal defect group was significantly less than that for the control group (mean ± SD, 61 ± 9 ml/m2versus 73 ± 13, p < 0.05) in keeping with previous studies. The slope of the log pressure-volume relation was significantly greater in the group with atrial septal defect than in the normal group (0.056 ± 0.010 versus 0.044 ± 0.008, p < 0.01), consistent with increased chamber stiffness.For a group of six patients with atrial septal defect and elevated left ventricular end-diastolic pressure, normalized compliance was significantly less than that in the control group (0.017 ± 0.001 versus 0.036 ± 0.007, p < 0.02). The slope k of the elastic stiffness-stress relation for the total group with atrial septal defect was significantly greater than that of the normal group (21.0 ± 2.3 versus 18.1 ± 2.3, p < 0.01). An index of muscle fiber stretch (dV/VdP × end-diastolic stress × 100) was significantly less in the atrial septal defect group than in the control group (74 ± 24 versus 106 ± 22, p < 0.01).Thus, left ventricular compliance and muscle stiffness may be adversely affected in atrial septal defect. Abnormal distensibility may exist in the presence of elevated left ventricular diastolic pressure and may have a rote in the genesis of left ventricular failure in this setting.