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At least 199 records · Page 11Linked to original sources
PubMed1991

[Hypertrophic myocardiopathy (I). The clinical and echocardiographic characteristics of a population of 72 patients].

The results of the echocardiographic evaluation of 72 patients with hypertrophic cardiomyopathy are presented. We have measured left ventricular wall thickness in 8 different segments and classified our patients in 6 types according to the hypertrophy extent. Moreover, we have evaluated by Doppler ultrasound the presence and severity of mitral regurgitation and the left ventricular inflow and outflow. The hypertrophy cardiomyopathy pattern was symmetric in 8 patients, apical in five, and asymmetric in 31. According to Maron classification, asymmetric cardiomyopathy was I type: 4 patients, II type: 16, III type: 11, and IV type: 0 patients. There were left ventricular outflow obstruction (greater than 25 mmHg) in 26 patients (36.1%). This obstruction was more frequent in II and III type hypertrophic cardiomyopathy and we found significative relationship between septal posterior segment hypertrophy and left ventricular outflow obstruction. Ventricular inflow showed bad distensibility pattern in 45 patients (62.5%). Mitral regurgitation was mild, moderate and severe in 25, 15, and 4 patients. Left ventricular outflow obstruction, bad distensibility pattern and mitral regurgitation were independent each other.

Adolescent↗
PubMed2006

Selective management of the left ventricular outflow tract for repair of interrupted aortic arch with ventricular septal defect: management of left ventricular outflow tract obstruction.

OBJECTIVE: Left ventricular outflow tract obstruction remains an early and late complication after repair of interrupted aortic arch and ventricular septal defect. We reviewed our experience with the selective management of the infundibular septum during primary repair to address left ventricular outflow tract obstruction. METHODS: From 1991 through 2001, all 27 patients presenting with interrupted aortic arch/ventricular septal defect and posterior deviation of the infundibular septum were analyzed. Fifteen patients with the smallest subaortic areas underwent myectomy or myotomy of the infundibular septum concomitant with interrupted aortic arch/ventricular septal defect repair. RESULTS: Patients undergoing myectomy-myotomy (Group I) had significantly smaller subaortic diameter indexes (0.83 +/- 0.16 cm/m2) when compared with those who had only interrupted aortic arch/ventricular septal defect repair (group 2: 0.99 +/- 0.13 cm/m2, P = .012). Two hospital deaths occurred in group 1, and 1 occurred in group 2. No late deaths occurred. No patient in group 2 required reoperation. Six group 1 patients required 9 reoperations for left ventricular outflow tract obstruction. Five patients underwent resection of a new subaortic membrane. Only 1 patient had recurrent muscular left ventricular outflow tract obstruction. Three patients required a second reoperation, primarily related to aortic valve stenosis. CONCLUSIONS: Interrupted aortic arch/ventricular septal defect with posterior malalignment of the infundibular septum can be repaired with low mortality in the neonatal period. Tailored to the degree of subaortic narrowing, resection or incision of the infundibular septum at the time of primary repair was very effective in preventing or prolonging the interval to recurrent left ventricular outflow tract obstruction compared with the published data. However, reoperation for left ventricular outflow tract obstruction, often related to the development of a new and discrete subaortic membrane or valvar stenosis, is still required in a subset of patients.

Aorta↗
PubMed1987

Evidence for true obstruction to left ventricular outflow in obstructive hypertrophic cardiomyopathy (muscular or hypertrophic subaortic stenosis).

In obstructive hypertrophic cardiomyopathy (muscular or hypertrophic subaortic stenosis), there is rapid early systolic ejection through an outflow tract that is narrowed by ventricular septal hypertrophy. This results in Venturi forces acting on the mitral leaflets, which cause mitral leaflet systolic anterior motion. Subsequent mitral leaflet-septal contact results in obstruction to left ventricular outflow and concomitant mitral regurgitation. Evidence is provided that the subaortic pressure gradient in obstructive hypertrophic cardiomyopathy reflects true obstruction to left ventricular outflow. It is important to distinguish this truly obstructive subaortic pressure gradient, due to mitral leaflet-septal contact, from an early systolic impulse gradient, as well as from the intraventricular pressure difference that may be encountered in midventricular obstruction or cavity obliteration.

Aortic Valve Stenosis↗
PubMed2001

Anteroapical stunning and left ventricular outflow tract obstruction.

Dynamic left ventricular outflow tract (LVOT) obstruction is typically observed in the setting of hypertrophic cardiomyopathy. It has also been reported with concentric LV hypertrophy, excessive sympathetic stimulation, and acute myocardial infarction. We describe 3 patients with chest discomfort after emotional stress, who had pronounced abnormalities on electrocardiograms, insignificant obstructive coronary disease and hemodynamic instability with LVOT obstruction, and regional wall motion abnormalities. Suppression of contractility with beta-blockers resulted in resolution of the gradient and in clinical improvement. On follow-up, functional recovery was excellent, and ventricular function had normalized. The conditions and mechanisms that may produce this sequence of events are discussed. The most probable scenario is that an acute ischemic insult secondary to vasospasm, LV stunning, and acute geometric remodeling produced a substrate for LVOT obstruction that was exacerbated by basal LV hypercontractility. The importance of this observation is that routine treatment of cardiogenic shock cannot be used and that conservative management results in excellent prognosis.

Aged↗
PubMed1986

Accessory mitral valve tissue causing left ventricular outflow tract obstruction.

Although left ventricular outflow tract obstruction is commonly associated with congenitally corrected transposition of the great vessels, this obstruction is seldom caused by accessory mitral valve tissue. Three cases in which accessory mitral valve tissue caused left ventricular outflow tract obstruction in children are described. Two had congenitally corrected transposition and one had normally connected great vessels. The accessory leaflet tissue, which was identified by echocardiography and angiography, was attached by chordae tendineae to normally sited papillary muscles and herniated into the left ventricular outflow tract during systole. Operation was successful in these patients. The accessory valve tissue was excised via an arteriotomy in the great vessel that arose from the left ventricle. The obstructive tissue was excised close to its peripheral attachments in the outflow tract and its chordae tendineae were divided. Resection was performed without injury to the abnormally placed conduction system or to the normal valve structures.

Adolescent↗
PubMedDate not supplied

Accessory mitral valve tissue: an increasingly recognized cause of left ventricular outflow tract obstruction.

Subvalvar left ventricular outflow tract obstruction (LVOTO) may be secondary to congenital abnormalities of the mitral valve, including abnormal attachments of the anterior leaflet of the mitral valve, parachute mitral valve, and accessory valve tissue. Successful correction of LVOTO due to accessory mitral valve tissue is reported in a 44-year-old man. Twenty-five patients with LVOTO due to accessory mitral valve tissue have been previously reported; however, only a few have been recognized preoperatively. A high index of suspicion is necessary for preoperative and intra-operative recognition and correction of the abnormality.

Adult↗