Acute chest pain and progressive dyspnea led to the admission of an 83-year-old female patient with known severely impaired left ventricular (LV) function and secondary mitral regurgitation II due to dilated cardiomyopathy (DCM). Recurrent decompensations had led to cardiac resynchronization therapy via defibrillator (CRTD) implantation. Present cardiovascular risk stratification revealed metabolic syndrome (obesity, diabetes mellitus type 2, arterial hypertension and hyperlipoproteinemia) complicated by previous stroke, whereas relevant coronary artery disease had been excluded years before. Moreover, recurrent exacerbating obstructive lung disease (COLD, GOLD III) was reported and advanced renal failure was documented [K/DOQI III, serum creatinine 2.2 mg/dL, urea 96 mg/dL, glomerular filtration rate (GFR, MDRD) 23 mL/min]. Initial clinical examination revealed wheezing over both lungs and mild edema of the lower limbs. There was sinus rhythm at a normal heart rate and bothsided blood pressure of 220/100 mmHg. Chest pain did not completely diminish, whereas myocardial infarction was ruled out using highly sensitive troponin T assay. The patient’s antihypertensive medication included seven substances with several second-line antihypertensives, all at high dose. Under additional intravenous (i.v.) nitrates, blood pressure remained merely controllable. With the addition of an oral central a-2 agonist and an oral reninreceptor antagonist, i.v. nitrates could be weaned (Table 1). In view of severely reduced glomerular filtration rate, the patient was refused to be treated with mineralocorticoidreceptor antagonist (MRA) as spironolactone or eplerenone, but left with sequential nephron blockade [1]. Coronary angiography demonstrated a high-grade stenosis of the left anterior descending coronary artery, contributing to recurrent angina pectoris. Percutaneous coronary intervention (PCI) was performed immediately. Post-PCI, we decided to angiographically search for underlying renal artery stenosis (RAS) in a hypertensive patient with continuously decreasing renal function and known coronary atherosclerosis. We demonstrated a highgrade RAS on the left (Fig. 1) and a rudimental renal artery on the right side. Further diagnostic workup including kidney ultrasound revealed a right-sided renal hypoplasia with no measurable resistance index (RI) and a normal appearing left kidney with a moderately reduced RI of 0.85. Thus, renal artery revascularization was considered, but defined as an ultima ratio after having exhausted all medical options. Under extended medical therapy (Table 1), the patient recurrently presented with blood pressures of up to 190/100 mmHg with accompanying angina and dyspnea due to flash pulmonary edema on days 4 and 7. Finally, stenting of the left renal artery was performed (Fig. 1). Hemodynamically relevant RAS (C70 % diameter stenosis) is one potential cause of secondary hypertension, also leading to impairment of renal function. Its diagnosis and its causal connection to hypertension and renal failure can be ambiguous. There are two underlying pathologies: 95 % of RAS is caused by atherosclerosis typically found at the proximal or ostial vessel. Fibromuscular dysplasia showing a string of beat pattern of the mid and/or distal renal artery is less T. Demming N. Frey C. Langer (&) Klinik fur Kardiologie und Angiologie, Universitares Gefaszentrum Nord, Universitatsklinikum Schleswig–Holstein, Campus Kiel, Christian-Albrechts Universitat Kiel, Schittenhelmstr. 12, 24105 Kiel, Germany e-mail: christoph.langer@uksh.de
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