_________________________________________________ From the Division of Cardiology, Department of Cardiac, Thoracic and Vascular Sciences, University of Padua, Padua, Italy. The authors report no conflicts of interest regarding the content herein. Manuscript submitted January 4, 2010 and accepted January 18, 2010. Address for correspondence: Giuseppe Tarantini, MD, PhD, Division of Cardiology, Department of Cardiac, Thoracic and Vascular Sciences, University of Padua, Via Giustiniani, 2, 35128 Padua (PD), Italy. E-mail: firstname.lastname@example.org
ABSTRACT:We report a case of pulmonary edema experienced in a patient with severe left ventricular dysfunction without an obvious cause. Thus, we tested the hypothesis of a dynamic increase in the severity of (ischemic) mitral regurgitation. Right-and left-heart cardiac catheterization was performed before and after 2 minutes of maximal handgrip. We observed an increase in the patient’s left ventricular systolic and end-diastolic pressures, his pulmonary and wedge capillary pressures, his heart rate and severe mitral regurgitation. J INVASIVE CARDIOL 2010;22:298–299 Key words: acute pulmonary edema; functional mitral regurgitation Case description. A 64-year-old male was admitted to the emergency department because of acute pulmonary edema. Eighteen years before admission, he had an inferior myocardial infarction (MI) treated with thrombolytic therapy, and 2 months later, he underwent triple coronary artery bypass graft surgery complicated by an anterior MI. Three years before the current admission, he underwent percutaneous coronary stenting of the saphenous graft for the obtuse marginal. The saphenous vein graft for the right coronary artery was occluded proximally. The patient complained of dyspnea (NYHA II) and asthenia until the day before the current admission. At admission, a physical examination revealed elevated jugular venous pressure; muffled S1, prominent P2; S3 gallop, apical low-intensity systolic blowing murmur radiating to the back, and 1+ pitting edema in both lower extremities. His systolic blood pressure was 170 mmHg. The electrocardiogram (ECG) showed sinus tachycardia (105 bpm), without new ST-segment or T-wave abnormalities. The patient’s troponin I peaked at 6 μg/L. His serum creatinine was normal. The NT-proBNP was 8,756 pg/mL. A chest X-ray showed enlargement of the peribronchiovascular spaces, Kerley B lines, acinar areas of increased opacity that coalesced into frank consolidations and enlargement of the cardiac silhouette. The patient was treated with oxygen, nitrates and furosemide. Three days after resolution of the acute pulmonary edema, the patient underwent coronary angiography, which revealed 3- vessel coronary disease with only 1 graft occluded (superimposable to a previous coronary angiography). At left ventricular angiography, a severe ventricular dysfunction with only mild mitral regurgitation was present (Figure 1). Pulmonary edema without an obvious cause experienced in a patient with severe left ventricular dysfunction has been shown to be related to a dynamic increase in the severity of (ischemic) mitral regurgitation.1 To test this hypothesis in our patient, we repeated during the same invasive examination right-and left-heart cardiac catheterization at 2 minutes of maximal handgrip to evaluate the changes in his hemodynamic parameters during the handgrip maneuvers. We observed an increase in the patient’s left ventricular systolic and end-diastolic pressures, his pulmonary and wedge capillary pressures, his heart rate, and a large increase in mitral regurgitation, as shown in Figure 1.
1. Pierard LA, Lancellotti P. The role of ischemic mitral regurgitation in the patho- genesis of acute pulmonary edema. N Engl J Med 2004;351:1627‚Äì1634.