Left ventricular (LV) answer to chronic pressure overload of aortic stenosis (AS) is usually characterized from an increase of wall thickness without cavity enlargement ("concentric hypertrophy") During follow-up sum of two units patients with AS developed relevant structural and functional changes of the left ventricle.

Left ventricular (LV) answer to chronic pressure overload of aortic stenosis (AS) is usually characterized from an increase of wall thickness without cavity enlargement ("concentric hypertrophy") During follow-up sum of two units patients with AS developed relevant structural and functional changes of the left ventricle, ie, progressive LV dilatation, wall thinning, and reduction of systolic performance. At the same time, the patients had clinical symptoms of congestive heart failure. The pathophysiologic relevance of this form of LV remodeling in AS is discussed.

Left ventricular (LV) concentric hypertrophy is the main adaptive mechanism to chronic urgency overload, such as valvular aortic stenosis (AS). The measurement of LV wall thickness by the agency of echocardiography commonly is used in patients with AS to assess noninvasively the hemodynamic load forward the left ventricle, thus indirectly estimating the severity of obstruction.[1] Furthermore, evidence exists that the progression of severity of AS usually is coupl with an increase in LV wall thickness. in succession the other hand, Bergeron and Schiller[2] lately reported two patients with rigorous AS and normal LV wall thickness. It is still unclear whether LV wall thinning personates a late stage of LV remodeling in AS or an abinitio different answer to chronic pressure overload. Here we describe 2 patients on the outside of a group of 45 make liables with AS serially evaluated through Doppler echocardiography[3] in whom progressive LV wall thinning and systolic dysfunction concomitantly with progression of stenosis were documented. To our knowledge, similar as phenomenon has not been previously described in humans.

CASE REPORTS

CASE 1

An 81-year-old man with lately diagnosed AS was admitted to our Department for the assessment of severity of valve disease. During his hospital stay, an episode of paroxysmal atrial fibrillation caused acute pulmonary edema and systemic hypotension. Doppler echocardiography documented a calcific aortic valve with a peak aortic velocity from continuous wave of 4 m/ corresponding to a peak crushing gradient of 64 mm Hg at modified Bernoulli equation; aortic area was approximately 1 [cmsup2] on continuity equation. The left ventricle was normal to small with significant wall hypertrophy (16 mm at close diastole). Left ventricular systolic function, asserted by fractional shortening on the transverse plane, was normal (fractional shortening: 40 percent; normal value, [greater than] 25 percent) The patient refused aortic valve replacement. At following evaluations, an increase in AS severity was observ together with a progressive increase in LV dimension and reduction of wall thickness and systolic function (Fig 1) Also the symptoms of heart failure reappeared and worsened in time. After 36 month of follow-up the patient was admitted again to the hospital with a clinical picture of austere congestive heart failure unresponsive to medical therapy. Echocardiography revealed a dilated left ventricle, and the interventricular septum and posterior wall had a normal end-diastolic thickness (11 mm) and were diffusely hypokinetic. As a issue global LV systolic function was markedly reduc Aortic area measured 05 [cmsup2] The patient still refused aortic surgery or balloon valvuloplasty and died a not many days later of refractory heart failure.

CASE 2

A 62-year-old man was referr to cardiologic evaluation in February 1988 because of a novel history of exercise-induced shortness of breath. in succession clinical examination, the heart was not enlarged with a sustained apical impulse; [Ssub2] was reduc and [Ssub4] was at hand A grade 3/6 systolic ejection whisper; low louder at the cardiac base and radiating to the neck was heard. The carotid fruit of leguminous plants rose slowly and a thrill was palpable. Electrocardiographic QR voltage criteria for LV hypertrophy were ready Echocardiography showed a normally sized left ventricle with moderate increase of end-diastolic wall thickness (14 mm); no regional asynergy in succession a two-dimensional tracing was seen and global LV systolic function was normal (Fig 1 and 2A). The aortic valve was tricuspid with calcified and rigid cusps. A peak velocity jet of 37 m/ was recorded through Doppler, corresponding to a peak constraining force gradient of 55 mm Hg; aortic area was 09 [cmsup2] Aortic valve surgery was praiseed but the patient refused, and therapy with calcium antagonists and nitrates was started.

During the nearest years, his clinical condition was stable, however the patient limited his physical activity. Serial echocardiograms showed an increase of valve stenosis severity; as in the previous patient, the left ventricle dilated and systolic function deteriorated progressively. In March 1990 previous therapy was withdrawn and treatment with furosemide and captopril was started. In July 1991 the patient was admitted to the hospital for rigid congestive heart failure (New York Heart Association class 4) Aortic valve area was 06 [cmsup2] by way of Doppler echocardiography. Echocardiography revealed a moderate LV dilatation, thin ventricular walls (end-diastolic thickness of 9 mm) with diffuse reduction of systolic thickening, and bitter impairment of global LV systolic function (Fig 2B) A 3+ mitral regurgitation was plant At coronary arteriography, a 50 percent stenosis of the right coronary artery and of a marginal branch of the left circumflex artery was institute The clinical condition improved with medical therapy, yet the patient died suddenly at dwelling 2 weeks later while waiting for cardiac surgery

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