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PubMedDate not supplied

[Transesophageal echocardiography in dynamic obstruction of left ventricular outflow after mitral valve surgery].

The authors report a case of dynamic obstruction of the ventricular outflow due to mitral valve surgery (valvuloplasty) in a 70-year-old woman with posterior leaflet mitral prolapse and severe regurgitation associated with anomalous implant of the posterior papillary muscle and increased thickness of the basal interventricular septum. Mitral valve surgery, possible for isolated prolapse of the LPM, although myectomy of the SIV has been performed, has determined onset of a systolic anterior motion (SAM), responsible of the dynamic obstruction. The diagnosis by means of transesophageal echocardiography (TEE) of the secondary SAM has allowed to optimise therapy (suspension of the inotropic drug, increase of volemia) with rapid improvement of hemodynamic conditions and in the following controls at is possible to observe a remodelling of the left ventricular geometry with pressure gradient reduction.

Aged↗
PubMed1998

Abnormal left ventricular filling after neonatal repair of congenital heart disease: association with increased mortality and morbidity.

BACKGROUND: The presence of mid-diastolic flow reversal on the mitral valve Doppler inflow indicates abnormal left ventricular filling. To determine whether mid-diastolic flow reversal predicts outcome in patients undergoing repair or palliation of neonatal congenital heart disease, we reviewed the echocardiograms and medical records of 40 patients with either left ventricular outflow obstruction or transposition of the great arteries. METHODS: All patients underwent surgical repair; transposition of the great arteries (TGA) = 17, coarctation of the aorta (CoA) = 14, interrupted aortic arch (IAA) = 8, and aortic stenosis (AS) = 1. The presence of mid-diastolic flow reversal was determined by pulsed Doppler interrogation of the mitral valve on preoperative and postoperative echocardiograms. RESULTS: Preoperative echocardiograms showed diastolic flow reversal in only 5 patients; 1 of 1 with AS and 4 of 14 with CoA. Twenty-one of 40 patients showed postoperative diastolic flow reversal; 1 of 1 with AS, 8 of 8 with IAA, 1 of 14 with CoA, and 11 of 17 with TGA. Postoperative mid-diastolic flow reversal 1 to 3 days after surgery was associated with higher mortality rate: 7 of 21 patients with diastolic flow reversal and 0 of 19 without diastolic flow reversal died. Patients with diastolic flow reversal who survived had longer intensive care unit (26.2 +/- 13.5 days vs 7.1 +/- 4.1 days, P <.001) and hospital (57.4 +/- 38.8 days vs 14.8 +/- 5.2 days, P <.05) stays. CONCLUSION: Mid-diastolic flow reversal is an indicator of prolonged hospital stay and mortality in patients with left ventricular outflow tract obstruction or TGA.

Diastole↗
PubMed1987

Dynamic obstruction to left ventricular outflow: the case for its existence in hypertrophic cardiomyopathy.

The debate and controversy over the hemodynamics of obstruction and left ventricular ejection in HCM is an interesting and complex one in which periodic disagreement has appeared during the last 20 years. We believe that the available data unequivocally support the concept that in those patients with HCM who have left ventricular outflow gradients measured at catheterization (and who have associated marked SAM) a mechanical impediment to forward flow, and thus true obstruction to left ventricular outflow, does exist. Most importantly, the gradient has critical clinical implications by virtue of the markedly elevated intraventricular systolic pressures associated with it. These chronically elevated pressures are potentially detrimental to the left ventricle (a view held even by investigators opposed to the term "obstruction"), by virtue of increasing systolic myocardial wall stress and myocardial oxygen demand. Therefore, surgical abolition of the obstruction and normalization of these pressures remains an important and rational therapeutic objective in those severely symptomatic patients who have obstruction to left ventricular outflow and who have failed to benefit from drug therapy.

Cardiomyopathy, Hypertrophic↗
PubMed1992

[Left intraventricular gradients measured by Doppler echocardiography at rest, during exercise and during isoproterenol test in hypertrophic cardiomyopathy].

Doppler echocardiography has been shown to be an accurate method of assessing left ventricular outflow obstruction in hypertrophic cardiomyopathy (HCM). One of the characteristics of this pressure gradient is its variability and, therefore, we measured this parameter during dynamic exercise testing in 33 patients. The results were compared with those recorded during isoproterenol infusion, the reference stress test for patients with HCM. Submaximal exercise in the recumbent position is usually well tolerated and resulted in a 43% increase in heart rate and a 47% increase in pressure gradient. There was a significant correlation between resting and exercise outflow obstruction (r = 0.90; p = 0.001). Moreover, exercise echo revealed obstruction in 26% of patients without resting pressure gradients (latent obstruction). The interpretation of results obtained with isoproterenol infusion is more difficult: this test resulted in an important increase in the left ventricular pressure gradient (231%) and "revealed" obstruction in 84% of cases. Therefore, we believe that exercise is more physiological and better tolerated than isoproterenol stress infusion and should be adopted as the investigation of choice in HCM even without obstruction at rest. If it is not possible to perform the exercise or no outflow tract obstruction can be demonstrated, an isoproterenol infusion may be used but this is not always well tolerated and the results should be interpreted with caution.

Cardiomyopathy, Hypertrophic↗
PubMed1994

[Mitral valve replacement and right ventricular outflow repair for hypertrophic obstructive cardiomyopathy].

A 44-year-old male with hypertrophic obstructive cardiomyopathy (HOCM) was operated on. He was in NYHA class III with a chief complaint of exertional dyspnea refractory to medical treatment. Echocardiography showed asymmetric septal hypertrophy and systolic anterior movement of the mitral valve, which caused obstruction of the left ventricular outflow tract. It also showed obstruction of the right ventricular outflow tract due to septal hypertrophy. Cardiac catheterization showed a systolic pressure gradient of 70 mmHg at the LV outflow tract and that of 30 mmHg at the RV outflow tract. He underwent mitral valve replacement and patch enlargement of the RV outflow tract. Postoperative course was uneventful. Postoperative catheterization showed a remarkable decrease of pressure gradient to 10 mmHg at the both outflow tracts.

Adult↗
PubMed1993

Reduction of the left-ventricular outflow-tract obstruction by aortoventriculoplasty--long-term results of 96 patients.

The aortoventriculoplasty (AVP) is an established surgical procedure for enlargement of different types of congenital and acquired obstruction of the left-ventricular outflow tract (LVOTO), especially with narrowing of the aortic valvular and subvalvular segment. Between 1974 and 1992, 96 patients underwent AVP. There were 32 female and 64 male patients, aged 3 to 32 years (mean 11.2 +/- 2.7 years) at operation. Indications for the procedure were as follows: 1. narrowing of the aortic annulus (19 patients), 2. multi-level stenosis (26 patients), 3. "outgrown"-prosthesis (8 patients), 4. recurrent hypertrophic obstructive cardiomyopathy (HOCM) (5 patients), and 5. subaortic stenosis of different origins (38 patients; out of these 19 patients had a "tunnel-like" stenosis, 7 of them with a "Shone-complex"). Seventy-six patients had previous operations at different levels of the left-ventricular tract. The mean preoperative peak transvalvular gradient was 88 +/- 27 mmHg (range 50-160 mmHg) and could be reduced by AVP to 14 +/- 13 mmHg. The early mortality was 8.3% (8/96). Among the last 58 patients there were no deaths. Three patients underwent subsequent reoperations: one for ascending aortic aneurysm, one for right-ventricular outflow tract obstruction (RVOTO), and one for "outgrown" prosthesis. Three patients required pacemaker implantation for a permanent a-v block, 71 of 96 patients had sinus rhythm postoperatively. The long-term results are similar to those of standard aortic valve replacement in childhood and adolescents. The advantages and disadvantages of the AVP in comparison to the other alternative surgical methods for relief of LVOTO are discussed.

Actuarial Analysis↗
PubMed1988

Noninvasive follow-up study in hypertrophic obstructive cardiomyopathy.

The clinical course of hypertrophic cardiomyopathy with left ventricular outflow obstruction showed a symptomatic progression in 25% of patients, independent of the of degree of left ventricular obstruction. Echocardiographic and mechanocardiographic examinations showed a close relationship between severity of asymmetric ventricular hypertrophy and diastolic failure. During the follow-up septal hypertrophy became more severe without left ventricular dilatation. Global diastolic function deteriorated and the left atrium dilated. The probability of survival was 67.2%. Our data suggest that septum hypertrophy and diastolic dysfunction are progressive in HOCM. The mortality is independent of the severity of hypertrophy and diastolic dysfunction, and shows a close correlation with arrhythmias.

Adult↗
PubMed2001

Natural history of hypertrophic cardiomyopathy: Japanese experience.

BACKGROUND AND OBJECTIVES: Most patients with hypertrophic cardiomyopathy (HCM) remain clinically stable for long periods of time, whereas some patients progress to severe systolic dysfunction. Therefore, the natural history of HCM is largely unknown. METHODS: The present study followed up 59 patients with HCM (32 males, 27 females, mean age 38.6 +/- 13.6 years) for 10 years or more (mean 16.0 +/- 4.7 years) after the initial diagnosis. RESULTS: Eight of 17 patients who showed abnormal Q-waves at the initial examination had lost Q-waves, suggesting remodeling from asymmetric to generalized hypertrophy. The thickness of the interventricular septum showed remarkable changes, increasing by > or = 5 mm in 7 patients and decreasing by > or = 5 mm in 21. These observations indicate that ventricular remodeling occurs in patients with HCM. Follow-up electrocardiography demonstrated new Q-waves in 10 patients and bundle branch blocks or intraventricular conduction disturbances in 13. Left ventricular end-diastolic diameter increased from 41.6 to 48.1 mm, associated with a decrease in fractional shortening from 40.6% to 34.0%. Left ventricular systolic dysfunction, defined as left ventricular end-diastolic diameter > 55 mm or fractional shortening < 25%, developed in 13 patients. These observations indicate that myocardial disease including the conduction system is progressive in patients with HCM and finally deteriorates to systolic dysfunction. Left ventricular outflow obstruction also presented evolutional changes. At the initial study, 23 patients showed systolic anterior motion of the mitral valves. Systolic anterior motion disappeared in 13 patients, reduced in 2, increased in 2, and remained stable in only 6. One patient without systolic anterior motion at the initial study developed new systolic anterior motion. Impaired left ventricular filling increased left atrial diameter from 35.5 to 46.9 mm and atrial fibrillation frequently developed (24 patients). CONCLUSIONS: These findings suggest that HCM is a slowly progressive disease which develops evolutional remodeling of left ventricular hypertrophy and outflow obstruction, eventually progressing to systolic dysfunction with cavity dilation and wall thinning.

Adult↗
PubMed2002

Management and outcome of patients with abnormal ventriculo-arterial connections and mitral valve cleft.

BACKGROUND: In patients with abnormal ventriculo-arterial connections, a mitral valve cleft different from an atrioventricular canal is occasionally associated. It may cause outflow obstruction, mitral regurgitation, and complicate biventricular repair. METHODS: A retrospective review identified 21 patients operated upon with mitral valve cleft, abnormal ventriculo-arterial connections, and two well-developed ventricles. Eight patients had a ventricular outflow obstruction due to the mitral valve, whereas 2 had more than mild mitral regurgitation. One patient required initial mitral valve surgery. Eleven patients underwent biventricular repair, associated with mitral valve repair in 2 cases: arterial switch operation (n = 4), Senning operation (n = 3) associated with an arterial switch operation in one case, intraventricular repair (n = 3), and Rastelli-type extracardiac conduit repair (n = 1). Single-ventricle palliation was preferred in 10 patients with major mitral valve straddling (n = 5), outflow tract obstruction (n = 2), and noncommitted or multiple VSDs (n = 3). RESULTS: There were three hospital deaths, two of which occurred after biventricular repair and one after an early reoperation after a bidirectional cavopulmonary anastomosis. Postoperatively after biventricular repair, 1 patient required permanent pacemaker implantation and 3 patients were reoperated on for subaortic stenosis (n = 1) and mitral regurgitation (n = 2), with one late death. By multivariate analysis, patients with a double-outlet right ventricle were at greater risk of death (p = 0.04). After a mean follow-up period of 60.7 months (+/- 68.6 months), 16 patients are in New York Heart Association (NYHA) class I. One patient with a moderate mitral regurgitation on Doppler study is in NYHA class II. CONCLUSIONS: The surgical management remains controversial in patients with abnormal ventriculo-arterial connections and mitral valve cleft. Biventricular repair may not always be feasible, especially in cases of complex intracardiac anatomy associated with mitral valve straddling. Single-ventricle palliation can be achieved in these patients, although it is unknown whether the long-term results are as good as those obtained with biventricular repair.

Adolescent↗
PubMedDate not supplied

Double-chambered right ventricle in an adult with Noonan syndrome.

We report the case of a double-chambered right ventricle in a 59-year-old man with previously undiagnosed Noonan syndrome. The patient presented with dyspnea on exertion and his transthoracic echocardiogram suggested a right ventricular outflow tract obstruction. Cardiac catheterization, cardiac magnetic resonance imaging, and transesophageal echocardiography revealed a hypertrophic muscle bundle dynamically obstructing right ventricular outflow. He was referred for operative repair of his double-chambered right ventricle and had successful patch expansion of his right ventricular outflow tract. In addition, he underwent a medical genetics evaluation that confirmed a new diagnosis of Noonan syndrome. To the best of our knowledge, this is the first report of a double-chambered right ventricle in an adult patient with Noonan syndrome.

Diagnosis, Differential↗
PubMed1980

Characterization of the cardiomyopathy in infants of diabetic mothers.

A transient form of hypertrophic cardiomyopathy has been previously described in infants of diabetic mothers (IDMs). The purpose of this study was to determine the incidence, natural history and pathologic features of this cardiomyopathy in symptomatic and asymptomatic IDMs. We studied 47 IDMs for evidence of cardiomyopathy. Among 24 symptomatic IDMs, five had marked septal hypertrophy with echocardiographic features suggesting left ventricular outflow obstruction and five had hypertrophy of the right ventricular free wall. With the exception of mild septal hypertrophy, these abnormalities resolved during the first 6 months of life, and echocardiograms in the first-degree family members were normal. Of 23 asymptomatic IDMs, three had septal hypertrophy and two had right ventricular free wall hypertrophy; none of the asymptomatic IDMs had evidence of outflow obstruction. One symptomatic IDM died, and autopsy revealed a hypertrophic septum that distorted both ventricular cavities. Microscopic examination revealed hypertrophic fibers and occasional areas of cellular disarray in the septum. Despite the clinical and pathologic similarities of the cardiomyopathy in IDMs to the hypertropic cardiomyopathies in older children and adults, its transient and nonfamilial nature suggest that it is a separate disease. We speculate that it is a manifestation of the generalized organomegaly in IDMs.

Aortic Valve Insufficiency↗
PubMed1988

Accessory valve cusp as a cause of outflow tract obstruction in atrio-ventricular and ventriculo-arterial discordance.

Congenital corrected transposition of the great arteries in which there is both an atrio-ventricular and a ventriculo-arterial discordance has surgical significance only in consequence of the associated cardiac anomalies. Their surgical correction is subject to multifarious problems. An exceedingly rare cause of a left-ventricular outflow tract obstruction erroneously interpreted preoperatively in an eight-year-old boy is reported. In an l-transposition with inversion of both ventricles, the diagnosis "valvular pulmonary stenosis" was made preoperatively. However, a normally arranged tricuspid pulmonary valve without stenosis was revealed intraoperatively. On the other hand, dystopic valvular tissue in the form of a monocuspid atrioventricular valve which was attached to an accessory papillary muscle with several tiny tendons was found below the pulmonary valve in the morphological left ventricle. The accessory valve cusp, which was the cause of the hemodynamically relevant subvalvular pulmonary stenosis, had no connection with the mitral valve. The abnormal valve cusp was resected without injuring the normal structures. The angiographic follow-up after one year no longer revealed any pressure gradient. This case report points out the possibility of an outflow tract obstruction caused by a complete accesory valve cusp.

Child↗
PubMed2003

Hypertrophic cardiomyopathy: state-of-the-art review, with focus on the management of outflow obstruction.

Significant advances in our understanding and management of hypertrophic cardiomyopathy have been made in the last decade, as the complex genetics and phenotype-genotype correlations that characterize the disease are gradually unravelled. The well-described clinical heterogeneity of hypertrophic cardiomyopathy is now understood to be based on profound genetic variability, with at least 10 genes and over 150 mutations implicated. Several new therapeutic tools have entered clinical practice. The implantable cardioverter-defibrillator is now strongly indicated in those at high risk of sudden arrhythmic death. Our ability to abort sudden death in this subgroup has placed added emphasis on risk stratification in newly diagnosed patients. New procedures have also been developed for the relief of outflow obstruction in patients with refractory symptoms and a significant subaortic outflow gradient. Although not as efficacious as the 'gold-standard' surgical myectomy-myotomy, dual-chamber pacemaker implantation can be of modest benefit in select patients. Percutaneous transluminal septal myocardial ablation is an emerging catheter-based procedure for the relief of left ventricular outflow obstruction. Long-term follow-up data are still awaited. However, intermediate-term results suggest equivalent efficacy to surgical myectomy-myotomy.

Algorithms↗
PubMed2006

Midventricular obstruction and clinical decision-making in obstructive hypertrophic cardiomyopathy.

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.

Adult↗
PubMed1994

Ventricular septal defect and left sided obstructive lesions in infants.

Infants born with ventricular septal defect and left sided obstructive lesions display a variety of pathophysiologic features. Some patients have relatively straightforward afterload- or preload-induced congestive heart failure, whereas others have a mixed pattern. The presence of patent ductus arteriosus may add to the left-to-right shunt, or when the physiology is that of preductal coarctation, may be associated with a small left ventricular chamber. Over the years, various management schemes have been devised for infants with ventricular septal defect and left sided obstructive lesions. These have continued to evolve as surgical skills and techniques have improved for the neonate. However, differences among medical centers remain in 1994 regarding the type and timing of various one- and two-stage repairs. Ventricular septal defect and coarctation or interrupted aortic arch, especially when associated with other types of left ventricular outflow obstruction remains a serious high-risk problem, but affected infants appear to have a better long-term prognosis today than in the past. Complete repair at the time of diagnosis in the neonate, regardless of whether associated obstructions are present, remains the gold standard. However, excellent results can be obtained by more conservative approaches to these lesions, especially if the ventricular septal defect is not unduly large. For patients with ventricular septal defect and mitral stenosis, a series of palliative procedures and operations are often required.

Aorta, Thoracic↗
PubMed2004

Plasma N-terminal pro-brain natriuretic peptide: a marker of left ventricular hypertrophy in hypertrophic cardiomyopathy.

BACKGROUND: B-type natriuretic peptide is secreted mainly in the left ventricle in response to elevated wall tension. Plasma levels of the peptide correlate positively with cardiac filling pressures, making it an excellent marker for the presence of left ventricular dysfunction. In hypertrophic cardiomyopathy, enhanced production of B-type natriuretic peptide is observed. However, the relationship of the various structural and functional features present in the disease with the high plasma levels described is not yet fully clarified. In the present study, we prospectively assessed in hypertrophic cardiomyopathy the relationship of plasma NT-proBNP levels with the extent of left ventricular hypertrophy, presence of left ventricular outflow obstruction and echocardiographic parameters of left ventricular diastolic function. METHODS: The study population included 190 individuals: 53 patients with hypertrophic cardiomyopathy and well-preserved left ventricular systolic function (group A), 92 healthy relatives with no disease expression (group B), and an additional group of 46 healthy volunteers (group C) as controls for NT-proBNP levels. Groups A and B were characterized clinically and by echocardiography and compared with each other. Plasma NT-proBNP levels were measured (ECLIA-Elecsys proBNP) and compared in the 3 groups of individuals included in the study. In hypertrophic cardiomyopathy patients, correlation was sought between NT-proBNP levels, NYHA functional class and echocardiographic data. RESULTS: Groups A and B differed (p < 0.001) in septal thickness, maximal wall thickness, left ventricular hypertrophy score, left atrial size, left atrial fractional shortening, derived transmitral filling indices and plasma NT-proBNP levels (group A: 909.9 +/- 1554.2 pg/ml; group B: 40.7 +/- 45.1 pg/ml). Left ventricular diastolic size and pulmonary venous flow velocity-derived indices were similar in the 2 groups. NT-proBNP levels in group B and C (39.4 +/- 34.5 pg/ml) were similar (p = NS). In hypertrophic cardiomyopathy patients, NT-proBNP levels correlate directly with NYHA functional class (r = 0.56, p < 0.001), septal thickness (r = 0.53, p < 0.001), maximal wall thickness (r = 0.59, p < 0.001), left ventricular hypertrophy score (r = 0.63, p < 0.001), left atrial size (r = 0.32, p = 0.023) and mitral deceleration time (r = 0.46, p = 0.001) and inversely with left atrial fractional shortening (r = -0.41, p = 0.005). Functional class also correlates directly with left ventricular hypertrophy score (r = 0.39, p = 0.006), with the most symptomatic patients having the highest scores. CONCLUSIONS: In hypertrophic cardiomyopathy, plasma NT-proBNP levels depend mainly on the severity of left ventricular hypertrophy rather than on the presence of obstruction. Measurement of the peptide may help in the clinical characterization and follow-up of patients with this disease.

Adolescent↗
PubMed2002

Congenital mitral-aortic discontinuity.

Mitral-aortic (M-A) discontinuity is an uncommonly observed congenital malformation. From the embryologic point of view, it is a failure of the superior endocardial cushion of the A-V canal reach and insert into the aortic root (the mitral-aortic fibrous trigone). It should be differentiated from aorto-left ventricular discontinuity, a complication of endocarditis with excavating abscesses without boundaries. In congenital mitral-aortic discontinuity, the anterior leaflet of the mitral valve fails to insert into the aortic root. We report our experience with 2 patients. In patient 1, the severe left ventricular outflow obstruction was mainly caused by the mobile anterior leaflet of the mitral valve.

Adult↗
PubMed2006

Cibenzoline improves coronary flow velocity reserve in patients with hypertrophic obstructive cardiomyopathy.

The effect of cibenzoline, a class-Ia antiarrhythmic drug, on coronary flow velocity reserve (CFVR) was examined in patients with hypertrophic cardiomyopathy using transthoracic Doppler echocardiography. Coronary flow velocity reserve was assessed in 11 patients with hypertrophic obstructive cardiomyopathy (HOCM) and 12 patients with hypertrophic nonobstructive cardiomyopathy (HNCM), before and after the intravenous administration of cibenzoline (1 mg/kg). Coronary hyperemia was induced by an intravenous infusion of adenosine triphosphate and CFVR was calculated as the ratio of hyperemic to basal mean coronary diastolic flow velocity. At baseline, CFVR was significantly correlated with left ventricular outflow tract pressure gradient (LVPG) in patients with HOCM (r = 0.67, P < 0.03). In patients with HOCM, administration of cibenzoline significantly improved impaired CFVR (2.0 +/- 0.8 to 3.0 +/- 1.0, P < 0.001), and reduced LVPG (55 +/- 30 to 23 +/- 18 mmHg, P < 0.001), while CFVR remained unchanged in patients with HNCM (2.6 +/- 0.9 to 2.9 +/- 0.8, P not significant). Cibenzoline not only reduces LVPG but also improves CFVR in patients with HOCM. In addition left ventricular outflow obstruction plays an important role in impaired coronary circulation in patients with HOCM.

Adenosine Triphosphate↗