PubMed · 9736474
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M R Bristow. 1998. Why does the myocardium fail? Insights from basic science.. https://doi.org/10.1016/s0140-6736(98)90311-7
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BACKGROUND: Elevated plasma endothelin-1 (ET-1) levels in patients with chronic heart failure correlate with pulmonary artery pressures and pulmonary vascular resistance. ET(A) receptors on vascular smooth muscle cells mediate pulmonary vascular contraction and hypertrophy. We determined the acute hemodynamic effects of sitaxsentan, a selective ET(A) receptor antagonist, in patients with chronic stable heart failure receiving conventional therapy. METHODS AND RESULTS: This multicenter, double-blind, placebo-controlled trial enrolled 48 patients with chronic New York Heart Association functional class III or IV heart failure (mean left ventricular ejection fraction 21+/-1%) treated with ACE inhibitors and diuretics. Patients with a baseline pulmonary capillary wedge pressure >/=15 mm Hg and a cardiac index </=2.5 L. min(-1). m(-2) were randomized to 1 of 3 doses (1.5, 3.0, or 6.0 mg/kg) of sitaxsentan or placebo as an intravenous infusion over 15 minutes. Hemodynamic responses were assessed by catheterization of the right side of the heart for 6 hours. Sitaxsentan decreased pulmonary artery systolic pressure, pulmonary vascular resistance, mean pulmonary artery pressure, and right atrial pressure (P</=0.001, 0.003, 0.017, and 0.031, respectively) but had no effect on heart rate, mean arterial pressure, pulmonary capillary wedge pressure, cardiac index, or systemic vascular resistance. Plasma ET-1 levels were elevated at baseline and decreased with sitaxsentan. CONCLUSIONS: In patients with moderate to severe heart failure receiving conventional therapy, acute ET(A) receptor blockade caused selective pulmonary vasodilation associated with a reduction in plasma ET-1. Sitaxsentan may be of value in the treatment of patients with pulmonary hypertension secondary to chronic heart failure.
A 56-year-old man presented with late cardiac tamponade appearing on 9 postoperative day after weaning from percutaneous cardiopulmonary support. He had been referred to our hospital for congestive heart failure. He underwent aortic valve replacement and fell into postcardiotomy low output syndrome. He could not be weaned from extracorporeal circulation, and we had to use an intraaortic balloon pump and percutaneous cardiopulmonary support. On postoperative day 9, percutaneous cardiopulmonary support was successfully withdrawn without problems, but he showed signs of superior vena cava syndrome after the cannulas were removed. An echocardiogram also showed cardiac tamponade. When the wound was reopened, a lot of old clots had compressed the right atrium and, after clot removal, the patient's hemodynamic state improved markedly. It is important to be aware that percutaneous cardiopulmonary support may conceal hemodynamic deterioration due to cardiac tamponade and to take care that a patient does not experience hemodynamic deterioration after percutaneous cardiopulmonary support withdrawal.
A low cardiac output state is an important cause of morbidity and mortality following repair of tetralogy of Fallot (ToF). This is often refractory to conventional measures. The cardiac output of these patients is highly dependent on diastolic pulmonary arterial flow which is enhanced during spontaneous respiration, but much reduced by intermittent positive pressure ventilation (IPPV). We report the successful use of negative pressure ventilation (NPV) as haemodynamic therapy in three children with a low output secondary to restrictive right ventricular (RV) physiology following ToF repair. NPV produced a significant haemodynamic improvement, with increases in cardiac output of greater than 100 % in two of the children. By augmenting pulmonary blood flow, and hence cardiac output, NPV has a role as adjunctive haemodynamic therapy in patients with a low output secondary to diastolic RV dysfunction, in whom early extubation is not possible.