Search

Purpose To investigate the safety and efficacy of the Parodi anti-embolism system (PAES) in establishing flow reversal in the internal carotid artery (ICA) as a means of protecting against embolic phenomena during carotid stenting. Methods Seven centers participated in a nonrandomized, prospective trial of carotid angioplasty and stenting under PAES protection in 30 patients (22 men; mean age 72 years, range 49-88) with 15 symptomatic (>70%) and 15 asymptomatic (>80%) stenotic ICAs. Safety was defined as achieving sufficient brain oxygenation during flow reversal as determined by level of awareness and motor control. The presence of new or enhanced neurological deficits and death were endpoints. Performance was based on angiographic evidence of successful retrograde flow. Results The PAES was positioned in all 30 patients, but technical error and access-related difficulties prevented establishment of reversed flow in 2. Among the 28 (93%) patients treated under PAES protection, 1 patient developed aphasia after flow reversal, necessitating balloon deflation between subsequent stages of the procedure. Three other adverse events included 1 case of bradycardia and 2 cases of hypotension, with dysarthria and facial paresis in one and temporary loss of consciousness in the other. All events resolved with appropriate therapy, and there was no change from baseline in the neurological status or brain scans at 24 hours. There were no strokes or neurological deficits at 30 days. Conclusions The PAES appears to be a safe and effective means of providing protection from embolic complications during carotid stenting.

Microvascular dysfunction can be demonstrated in most patients with hypertrophic cardiomyopathy (HCM), both in the hypertrophied and nonhypertrophied myocardial walls, mostly due to intimal and medial hyperplasia of the intramural coronary arteries and subsequent lumen reduction. As a consequence, regional myocardial ischemia may be triggered by exercise, increased heart rate, or arrhythmias, in areas which are unable to increase myocardial blood flow. In patients with HCM, microvascular dysfunction leading to severe myocardial hypoperfusion during maximal hyperemia represents a strong predictor of unfavorable outcome, left ventricular remodeling with progressive wall thinning, left ventricular dysfunction, and heart failure. Accurate quantitative assessment of microvascular dysfunction and myocardial ischemia is not easily feasible in clinical practice. Although signs of inducible myocardial ischemia may be detected by electrocardiogram, echocardiography, or myocardial scintigraphy, the vasodilator response to dipyridamole by positron emission tomography is considered the method of choice for the assessment of maximal regional and global flow. Cardiac magnetic resonance provides further information, by late gadolinium enhancement (LGE), which may show areas where replacement fibrosis has occurred following microvascular ischemia and focal necrosis. LGE areas colocalize with severe regional microvascular dysfunction, are associated with increased prevalence of ventricular arrhythmias, and show more extensive distribution in the late stages of the disease, when heart failure is the dominant feature. The present review aims to provide a concise overview of the available evidence of microvascular dysfunction and ischemia eventually leading to disease progression and heart failure in HCM patients.

The presence of intraventricular obstruction is a powerful predictor of outcome in patients with hypertrophic cardiomyopathy (HCM) and, when associated with severe, drug-refractory symptoms, should be managed aggressively. Resting left ventricular outflow obstruction is found in approximately 20% of the patients, classically occurs at the subaortic level, and is associated with mitral valve systolic anterior motion (SAM). In a minority of patients, however, the impedance to flow occurs at midventricular level, unrelated to SAM. Symptomatic midventricular obstruction represents a clinical challenge, and its treatment is not standardized. In these patients, both surgical myectomy and alcohol septal ablation (ASA) are technically feasible. A rational approach to the management of these patients depends on accurate characterization of the pathophysiology, coupled with comparison of the results of different management strategies. To illustrate these points, the details of a patient who first underwent percutaneous ASA and subsequently required redo surgical treatment are described here, with special emphasis on the implications to the management of midventricular obstruction, as well as to the more global issue of obstructive HCM.