Background: Anomalies of the mitral apparatus have been shown to contribute to left ventricular outflow obstruction in patients with hypertrophic cardiomyopathy (HCM). We report our 5-year single-center experience with a shallow myectomy procedure associated with transaortic mitral valve repair in a cohort of HCM patients. Methods: We studied 83 consecutive patients who underwent surgical treatment of symptomatic left ventricular outflow obstruction. In all study patients, a transaortic shallow septal myectomy was performed. Fibrous or muscular structures connecting the papillary muscles to the septum or free wall were resected, and fibrotic secondary chordae of the anterior mitral valve were cut selectively. Results: We report one death (1.2%) during hospitalization, no iatrogenic ventricular septal defects, and two (2.4%) mitral valve replacements. At discharge, no patients were in New York Heart Association (NYHA) Class III/IV, from 49 (59%) preoperatively. Mean maximal septal thickness decreased from 24 ± 6 to 16 ± 3 mm. Mean outflow gradient decreased from 93 ± 33 to 13 ± 11 mmHg. Grade 3 or 4 mitral regurgitation was noticed in one patient postoperatively, from 32 (39%) before surgery. Conclusions: Shallow septal myectomy associated with secondary mitral valve chordal cutting and papillary muscle mobilization provided excellent results offering adequate treatment of outflow obstruction.
Left ventricular pseudoaneurysm is a rare disease; it is defined as a ventricular rupture contained by epicardium, pericardial adhesions, or both. It most frequently occurs as a complication of acute myocardial infarction. Surgical treatment is recommended for pseudoaneurysms that are large or symptomatic and for those discovered less than 3 months after myocardial infarction. We report our experience with 2 patients who had left ventricular pseudoaneurysms discovered less than a week after inferior myocardial infarction. Both patients were middle-aged men with right coronary occlusion in whom the diagnoses were established by echocardiography during the first week after infarction. Because both patients were clinically stable, we opted to defer surgery until scarring could facilitate correction; this decision was based on a review of the literature showing that in-hospital mortality is higher with early surgery. The patients were monitored closely in the intensive care unit and were prescribed β-blockers and vasodilators. Both patients underwent left ventricular patch reconstruction with exclusion of the pseudoaneurysm and posterior septum; both received moderate inotropic support and prophylactic intra-aortic balloon pump assistance. Their postoperative courses were uneventful. In 5 prior reports describing 45 patients (13 with acute pseudoaneurysm [≤2 wk after infarction] and 32 with nonacute pseudoaneurysm), in-hospital mortality was 61.5% for patients in the acute group and 15.6% for the nonacute group (P = .0066). We recommend that clinicians consider deferring surgery for patients with stable acute left ventricular pseudoaneurysm to reduce the risks associated with early repair.
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