Literature DB >> 15908482

Impaired coronary and myocardial flow in severe aortic stenosis is associated with increased apoptosis: a transthoracic Doppler and myocardial contrast echocardiography study.

L Galiuto1, M Lotrionte, F Crea, A Anselmi, G G L Biondi-Zoccai, F De Giorgio, A Baldi, F Baldi, G Possati, M Gaudino, G W Vetrovec, A Abbate.   

Abstract

OBJECTIVE: To test the hypothesis that impaired coronary and myocardial blood flow are linked with increased myocyte apoptosis, thus establishing a link between pressure overload and left ventricular (LV) remodelling. METHODS AND
RESULTS: Peak diastolic coronary blood flow velocity (CBFV) was evaluated at transthoracic Doppler echocardiography, and signal intensity (SI) and the rate of SI rise (beta) were measured at myocardial contrast echocardiography in 11 patients with severe aortic stenosis and LV hypertrophy. In the same patients, biopsies were obtained from the anterolateral LV free wall during surgery and analysed for cardiomyocyte apoptosis. LV mass corrected CBFV (CBFVI) was significantly lower in patients than in controls (median 0.100 cm.g/s (interquartile range 0.07-0.115) v 0.130 cm.g/s (0.130-0.160), p = 0.002). Similarly, SI*beta was significantly lower in patients than in controls (11 1/s (8-66) v 83 1/s (73-95), p = 0.001). Apoptotic rate was increased in aortic stenosis more than 100-fold versus controls (1.2% (0.8-1.4) v 0.01% (0.01-0.01), p < 0.001) and inversely correlated with lower CBFVI and SI*beta (r = -0.77, p = 0.001 for both).
CONCLUSIONS: Patients with severe aortic stenosis and LV hypertrophy have impaired myocardial perfusion, which is associated with enhanced cardiomyocyte apoptosis. Impaired myocardial perfusion and the ensuing oxygen demand-supply imbalance may, at least partially, be responsible for increased apoptosis and possible transition to heart failure, thus establishing a link between pressure overload, LV remodelling, and heart failure.

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Year:  2005        PMID: 15908482      PMCID: PMC1860772          DOI: 10.1136/hrt.2005.062422

Source DB:  PubMed          Journal:  Heart        ISSN: 1355-6037            Impact factor:   5.994


  23 in total

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2.  Myocyte apoptosis and reduced SR gene expression precede the transition from chronically stunned to hibernating myocardium.

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Review 3.  Clinical practice. Aortic stenosis.

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4.  On the nature of cell death during remodeling of hypertrophied human myocardium.

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5.  Mechanisms of coronary microcirculatory dysfunction in patients with aortic stenosis and angiographically normal coronary arteries.

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6.  Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post-infarction heart failure.

Authors:  Antonio Abbate; Giuseppe G L Biondi-Zoccai; Rossana Bussani; Aldo Dobrina; Debora Camilot; Florinda Feroce; Raffaele Rossiello; Feliciano Baldi; Furio Silvestri; Luigi M Biasucci; Alfonso Baldi
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Review 7.  Pathophysiologic role of myocardial apoptosis in post-infarction left ventricular remodeling.

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9.  A mechanistic role for cardiac myocyte apoptosis in heart failure.

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10.  Temporal evolution and functional outcome of no reflow: sustained and spontaneously reversible patterns following successful coronary recanalisation.

Authors:  L Galiuto; A Lombardo; A Maseri; L Santoro; I Porto; D Cianflone; A G Rebuzzi; F Crea
Journal:  Heart       Date:  2003-07       Impact factor: 5.994

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Review 6.  Myocardial hypertrophy and its role in heart failure with preserved ejection fraction.

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7.  Determinants and Prognostic Significance of Symptomatic Status in Patients with Moderately Dysfunctional Bicuspid Aortic Valves.

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Review 10.  Role of advanced left ventricular imaging in adults with aortic stenosis.

Authors:  Andreea Calin; Anca D Mateescu; Andreea C Popescu; Rong Bing; Marc R Dweck; Bogdan A Popescu
Journal:  Heart       Date:  2020-03-16       Impact factor: 5.994

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