Microvascular Permeability Changes Might Explain Cardiac Tamponade after Alcohol Septal Ablation for Hypertrophic Cardiomyopathy

Abstract

P ercutaneous transluminal alcohol septal ablation (ASA), introduced in 1995, mimics surgical myectomy in that it reduces the left ventricular outflow tract (LVOT) gradient.1 The procedure has become widely used, and it is estimated that ASA therapies exceed myectomy procedures by 9-fold in the treatment of patients with symptomatic hypertrophic obstructive cardiomyopathy.2 A mean early mortality rate of 1.5% ± 0.03% in ASA has been reported (range, 0-5%).3 The reported sequelae of ASA include conduction disturbances, ventricular arrhythmias, coronary dissection, alcohol spillover into the left anterior descending coronary artery, post-myocardial infarction ventricular septal defect, right ventricular infarction, and cardiac tamponade. 3,4We describe the case of a patient in whom cardiac tamponade rapidly developed one hour after ASA, and we speculate on the cause of that massive pericardial effusion. Case ReportIn February 2010, a 78-year-old woman with type 2 diabetes mellitus and a history of hypertension controlled with diuretics was admitted to our hospital with acute pulmonary edema. Ventilatory support with bilevel positive airway pressure was rapidly implemented. Auscultation revealed an S 4 , a grade 3/6 systolic ejection murmur along the left and upper right sternal border, and a grade 3/6 apical pansystolic murmur that radiated to the axilla. Rapid elevation of the patient's cardiac troponin I level was detected, and an electrocardiogram (ECG) showed ST-segment depression in leads V 3 through V 6 (Fig. 1). The presumptive diagnosis was non-ST-elevation myocardial infarction. Emergent coronary angiography yielded patent coronary arteries and normal left ventricular wall motion. A transthoracic echocardiogram showed asymmetric hypertrophic cardiomyopathy (23-mm septal thickness and 8-mm lateral-wall thickness), with a peak instantaneous resting LVOT gradient of 172 mmHg and systolic anterior motion of the mitral leaflet. The resting LVOT gradient decreased to 52 mmHg after normal saline hydration and low-dose β-blocker therapy (Fig. 2A); however, the patient could not be weaned from mechanical ventilation. Substantial mitral regurgitation persisted after the hydration (Fig. 2B).During left-sided heart catheterization for ASA, the resting peak-to-peak gradient was 40 mmHg. We noted a post-premature ventricular capture beat and a prominent Case Reports

Predictive Factors of Pericardial Effusion After a First Acute Myocardial Infarction and Successful Reperfusion

“…1e3 Still, PE should be considered a risk factor for acute or subacute left ventricular (LV) free wall rupture, potentially resulting in tamponade and sudden cardiac death. Many parameters that may increase vascular permeability 4,5 have been suggested, such as intensity of myocardial injury, 3 increase in LV filling pressures, 6e8 or microvessel injury and endothelial dysfunction. 9,10 Microvascular obstruction (MVO) has, indeed, been associated with higher occurrence of PE or wall rupture.…”