PressureWire for Comprehensive Hemodynamic Assessment in a Patient with Mechanical Aortic and Mitral Valves

ABSTRACT: This is a case of a 65-year-old male with history of double mechanical valve implantation (aortic and mitral) who presented with symptoms of severe volume overload either related to cardiac disease or underlying cirrhosis. The precise etiology could not be determined by clinical examination and noninvasive diagnostic tests. A cardiac catheterization was deemed necessary to better clarify the diagnosis. Because of the presence of double mechanical valves, crossing the valves with a pigtail catheter and the 0.035-inch wire is contraindicated, traditionally necessitating transapical left ventricular puncture. The pressure wire is an intracoronary wire with a transducer affixed to its distal portion which is indicated for fractional flow reserve determination. We decided to use it in our patient as an off-label indication to cross the mechanical aortic valve safely and record all necessary hemodynamic measurements. Figures are shown of the comparisons between different intracardiac chambers in order to arrive at a final diagnosis without transapical puncture. J INVASIVE CARDIOL 2010;22:555–556 ———————————————————— Case description. A 65-year-old male presented with weakness, dyspnea on exertion, significant edema, abdominal distension and associated weight gain of 60 pounds over 2 months. His past medical history was remarkable for chronic alcohol use, atrial fibrillation and mechanical aortic and mitral valve replacement 8 years previously. Physical examination revealed jugular venous distension, ascites and 3+ pitting bilateral edema. On lung examination, there were bilateral basal crackles, while cardiac evaluation revealed a rapid irregular rhythm at 110 beats/min and audible clicks of the mechanical valves. Laboratory studies were remarkable for anemia (hemoglobin 8.2 g/dl), renal insufficiency (creatinine 3.1 mg/dL), and elevated liver function tests (SGOT 46 IU/L [N 13–39 IU/L], SGPT 43 IU/L [N 4–36 IU/L], Alk. phos 183 IU/L [N 25–100 IU/L, Total bilirubin 1.9 mg/dL (N 0.2–1.1 mg/dL], albumin 2.4 gm/dL [N 3.5–4.8 gm/dL]). Echocardiography showed severe concentric left ventricular hypertrophy (thickness 2.1 cm), a gradient across the mechanical aortic valve of 20 mmHg, and across the mechanical mitral valve of 9 mmHg, consistent with late-presenting mechanical valve stenoses. There was moderate-to-severe four-chamber enlargement, moderate tricuspid and pulmonic regurgitation and severe pulmonary hypertension (estimated 65 mmHg). The etiology of subacute clinical deterioration remained unclear despite prolonged hospitalization, and diuresis resulted in worsening renal failure and borderline hypotension. It remained difficult to determine whether the patient’s deterioration was due to cirrhosis or congestive heart failure, and if the latter, whether it was due to constrictive pericarditis (from a prior pericardiotomy), mechanical valve stenosis, severe diastolic dysfunction or primary pulmonary hypertension. An invasive test such as right and left heart cardiac catheterization was contemplated, although historically required transapical left ventricular puncture to measure end-diastolic pressure. A decision was made to perform comprehensive right and left heart cardiac catheterization using the 0.014 mm PressureWire (Volcano Corp., San Diego, California), indicated for fractional flow reserve (FFR) estimation. Fluoroscopy showed well-seated mechanical aortic and mitral valves with normal leaflet excursion. Right-heart hemodynamics revealed severe pulmonary hypertension (PASP 71 mmHg, mean 52 mmHg), severely elevated right and left atrial pressure (30 and 31 mmHg, respectively), mildly elevated pulmonary vascular resistance (PVR: 2.4 Woods units [N: 1.25–2.5 Woods units]), elevated cardiac output and cardiac index (CO: 8.5 l/min, CI: 3.38 l/min/m²) and low systemic vascular resistance (SVR: 6.9 Woods units [N: 11.25–15 Woods units]). The PressureWire passed across the mechanical aortic valve without difficulty, revealing physiologically insignificant gradients across both the aortic and mitral mechanical valves, and no evidence of constrictive pericarditis (concordant biventricular tracings) (Figure 1, A–D). Small gradients across both valves were consistent with normal mechanical valve physiology as well as superimposed volume overload. His hemodynamics were thus consistent with a chronic low systemic vascular resistance state and secondary volume overload, a picture consistent with the diagnosis of cirrhosis and hepatorenal syndrome. The patient was treated accordingly, with clinical improvement. We believe this to be the first reported case of comprehensive hemodynamic assessment of valvular stenosis and constrictive pericarditis in a patient with double mechanical valves using the PressureWire. Since transapical puncture is historically,^1,2 and currently, the only other viable alternative, we believe use of the Pressure Wire will become the default invasive strategy for assessment of these patients. The authors are not suggesting that this become a “clinical standard” — in fact, the echocardiogram should be able to fully assess prosthetic valve function without the need for an invasive assessment. However, in equivocal cases such as the one described here, this approach might add very useful information.

References

1. Baxley WA, Soto B. Hemodynamic evaluation of patients with combined mitral and aortic prostheses. Am J Cardiol 1980;45:42–47. 2. Rigaud M, Dubourg O, Luwaert R, et al. Retrograde catheterization of left ventricle through mechanical aortic prostheses. Eur Heart J 1987;8:689–696.

———————————————————— From the Department of Medicine, Division of Cardiology, Winthrop University Hospital, Mineola, New York. The authors report no conflicts of interest regarding the content herein. Manuscript submitted July 29, 2010, provisional acceptance given August 27, 2010, final version accepted August 31, 2010. Address for correspondence: Srihari S. Naidu, MD, FACC, FSCAI, Director, Cardiac Catheterization Laboratory, Winthrop University Hospital, 120 Mineola Blvd, Suite 500, Mineola, NY 11501. E-mail ssnaidu@winthrop.org