Background-The ability of the Naughton-Balke exercise treadmill test, an objective indicator of exercise capacity, to predict abnormal hemodynamics and mortality in pulmonary hypertension is unknown. Methods and Results-We performed a cohort study of 603 patients with pulmonary hypertension from 1982 to 2006, and studied the utility of exercise treadmill test as a predictor of abnormal hemodynamics and death. We used multivariable linear regression to determine whether exercise capacity, measured in metabolic equivalents, was associated with abnormal hemodynamics, and we used a Cox proportional hazards model to determine whether decreased exercise capacity predicted death. Mean age was 50Ϯ15 years, 76% were women, 63% had World Health Organization category I pulmonary arterial hypertension, and 23% were World Health Organization functional classes I and II. Mean exercise capacity was 3.7Ϯ2.2 metabolic equivalents. Decreased exercise capacity was independently associated with elevated right atrial and mean pulmonary artery pressure, decreased cardiac index, and increased pulmonary vascular resistance. During median follow-up of 4.6 years, 36% of the patients died. Decreased exercise capacity was associated with mortality (multivariable hazard ratio, 1.18; 95% CI, 1.01 to 1.37 for each 1-metabolic equivalent decrease in exercise capacity; Pϭ0.031; Pϭ0.052 after adjusting for invasive hemodynamic variables). Decreased exercise capacity also predicted mortality in functional classes I-II patients, 24% of whom died (hazard ratio, 1.53; 95% CI, 1.04 to 2.26 for each 1-metabolic equivalent decrease in exercise capacity; Pϭ0.032), although this association did not persist after adjusting for invasive hemodynamic variables (Pϭ0.63). Conclusions-Reduced exercise capacity on exercise treadmill test is associated with worse hemodynamics and is a predictor of mortality in patients with pulmonary hypertension. (Circ Heart Fail. 2009;2:278-286.)
Acute massive pulmonary embolism can have significant hemodynamic effects in both adults and children. We describe the case of a 10-year-old boy who developed cardiogenic shock after suffering a massive pulmonary embolism. A significant thrombus burden was removed using a catheter-based strategy of rheolytic thrombectomy, leading to stabilization of the patient.
The use of the Tandem Heart percutaneous ventricular assist device (Tandem Heart pVAD, Cardiac Assist technologies, Pittsburgh, PA) as a bridge to recovery or to other cardiopulmonary support systems has been rising. One requirement for placement of this device is an intraatrial septostomy which is usually closed during the surgical insertion of more permanent ventricular assist devices. We present a case of a 62-year-old man with a residual acquired atrial septal defect (ASD) from Tandem Heart placement, which could not be closed surgically during insertion of left and right ventricular assist devices. The patient remained intubated and hypoxemic after removal of his right ventricular assist device due to the presence of persistent right to left shunting. With closure of the ASD using an 8-mm Amplatzer septal occluder (ASO; AGA Medical Corp., Golden Valley, MN) the patient stabilized and was successfully extubated.
HighlightsTraumatic coronary artery-cameral fistula (TCAF) is rare after blunt chest trauma.Development of coronary steal and reversible ischemia can occur with TCAF.Disease can progress to cardiomyopathy and heart failure.Treatment involves early diagnosis with transcatheter or surgical interventions for ligation and revascularization.
Patients with pulmonary arterial hypertension (PAH) are often treated with parenteral prostanoids. Continuous infusion of parenteral prostanoids comes at the cost of increased risk of thromboembolism, bloodstream infections, and inconvenience to patient lifestyle. Patients with stable symptoms may be transitioned to an oral formulation of prostanoids. This transition has been accomplished safely over 5 days in prior studies. We present a protocol for safe and efficient transition from parenteral to oral prostanoids within 24 hours.
METHODS:We selected patients diagnosed with PAH who were started on continuous parenteral prostanoid therapy and subsequently stabilized symptomatically. Patients were electively admitted to the hospital for transition. The initial total daily dosage (TDD) of oral treprostinil was determined using the following equation: Oral treprostinil total daily dose (in mg) ¼ 0.0072 x parenteral treprostinil rate (in ng/kg/min) x weight (in kg). The TDD/3 yields the dose for three times daily dosing. Patients were transitioned off parenteral and onto oral treprostinil therapy within 24 hours using the following transition protocol.
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