Abstract

Abstract A 42 year-old woman presented with moderate exertion dyspnea within the past months. She was hypertensive, with end stage-chronic kidney disease (CKD) on hemodialysis for 8 years, initially by arteriovenous fistula and then by central venous catheter. She associated thrombosis of both common femoral veins. Clinical examination revealed mild leg edema, hepatomegaly, III/VI systolic murmur, left brachiocephalic arteriovenous fistula with aneurismal dilation and subclavian central venous catheter. Resting ECG showed atrial flutter with variable block and biventricular hypertrophy. Lab studies highlighted mild anemia, glomerular filtration rate (MDRD) 13.5 ml/min/1.73m2, hyperhomocysteinemia. Transthoracic echocardiography revealed left ventricle (LV) with normal diameters and mild concentric hypertrophy, mild systolic LV dysfunction and diastolic dysfunction (Fig A), dilation of both atria, mild mitral regurgitation, dilated RV with moderate global dysfunction, moderate tricuspid regurgitation and secondary pulmonary hypertension (PH) with estimated systolic pulmonary artery pressure of 79 mmHg (Fig C), moderate pulmonary regurgitation, moderate dilatation of pulmonary artery. Vascular Doppler ultrasonography showed thrombosis of the arteriovenous fistula and of right jugular vein. To confirm PH, right heart catheterization was necessary. The intervention could not be realized on femoral approach due to thrombosis of both common femoral veins. We considered the jugular approach, but weighing the risks/benefits balance, with one functional jugular vein, we decided not going for it, as the jugular approach was the only vascular approach for dialysis. We performed left catheterization right after a dialysis session and an LV end-diastolic pressure of 13 mmHg was measured. The possible causes of PH considered in this case were the CKD by itself, a pulmonary thromboembolic component in a patient with hyperhomocisteinemia and thrombosis of both femoral veins and a left heart component given the borderline value of LV end-diastolic pressure. The patient received treatment with beta-blockers, blockers of the renin-angiotenins-aldosterone system, calcium channel blockers and oral anticoagulation. She was evaluated after two months describing improvement of symptoms. The resting ECG showed sinus rhythm and the echocardiography revealed improved parameters of LV diastolic function (Fig B), with reduction of systolic pulmonary artery pressure (Fig D) and improvement of right heart parameters. PH is a frequent complication in patients with CKD on hemodialysis. Possible mechanism of its development include RV overload with increased pulmonary flow or creating a fistula with an increased flow through arteriovenous shunt. Thromboembolic complications and hyperhomocysteinemia are other frequent findings in these patients. Despite all the above, the left heart involvement with LV diastolic dysfunction remains a common and amendable cause of PH in this setting. Abstract P1687 Figure.

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