1

Introduction

Connections between heart and kidney are usually referred to pathophysiological relationships between heart failure and renal failure, but sometimes, connections between disease of both organs have unusual pathways. We present an intriguing case of connection between coronary artery disease and renal ischemia by means of paradoxical embolism via patent foramen ovale (PFO).

2

Case report

A 50-year-old female with no cardiovascular risk factors, presented to our service for urgent coronary angiography because of an acute coronary syndrome with electrocardiographic inferior ST elevation. At admittance the patient lamented intense chest pain and moderate back pain, blood pressure was 190/110 mmHg with a heart rate of 98 bpm. No high blood pressure was reported in the previous history of the patient, who played tennis and was regularly followed by the sport physician of her tennis club. The clinical examination was normal; in particular peripheral pulses were symmetric. A mild ematuria was present, initially ascribed to urinary catheter placement during emergency.

The coronary angiography revealed the likely occlusion of a small distal branch of the posterior interventricular artery in the total absence of even mild coronary atherosclerosis. A concomitant regional akinesia of the distal inferior left ventricular wall was seen at the left ventricular angiography. Due to the very small diameter of the culprit vessel, we decided to refer the patient to medical therapy with double antiplatelet therapy with aspirin and clopidogrel ( Fig. 1 A ).

(A) First coronary artery angiogram a small branch of the posterior interventricular coronary artery seemed to be occluded (arrow). (B) The second coronary angiogram at two days from admittance: now is evident the dissection of the vessel partially recanalized (arrow).

At the end of the procedure the patient was hypertensive despite therapy with nitrates and symptomatic mostly for intense right side back pain: a computed tomographic (CT) scan resulted negative for aortic dissection but revealed a small right cortical renal infarct ( Fig. 2 ). A rise in creatinine, in that case, greater than 25% (0.3 mg/dl) from baseline, documented a condition of Acute Kidney Injury (AKI) class “R” (AKIN stage 1).

The CT scan revealed the right renal cortical infarct (red circle).

Two days after, a new coronary angiography was undertaken to control the right coronary artery and this time the branch of the posterior interventricular coronary, considered the culprit vessel at the first angiogram, appeared as a dissection of a branch of moderate calibre ( Fig. 1 B).

During the following stay in hospital, the patient underwent an echocardiogram that confirmed a distal inferior left ventricular wall akinesia with a preserved left ventricular ejection fraction but, more interestingly, revealed a PFO. There was a small basal right to left shunt becoming massive after Valsalva manoeuvre and a moderate atrial septal aneurysm. The peak of Troponin I was 8.7 μg/l at 18 h. Subsequent evaluation of abnormalities of the coagulation cascade revealed only a mild hyperhomocisteinemia, whereas a venous Doppler ultrasound excluded deep vein thrombosis of the lower limbs.

Based on reported findings we postulated that a paradoxical embolism trough the PFO caused the renal infarct and a subsequent hypertensive crisis-induced coronary artery dissection. The patient now is under evaluation for trans-catheter closure of PFO.