scholarly journals Response of hypertrophied myocardium to ischemia

1981 ◽  
Vol 81 (6) ◽  
pp. 865-872 ◽  
Author(s):  
James D. Sink ◽  
Gary L. Pellom ◽  
William D. Currie ◽  
Ronald C. Hill ◽  
Craig O. Olsen ◽  
...  
Keyword(s):  
Hypertrophied Myocardium

scholarly journals Hypertrophic cardiomyopathy with paroxysmal atrial fibrillation misdiagnosed as WPW syndrome

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Sang-Hoon Seol ◽  
Ki-Hun Kim ◽  
Jino Park ◽  
Yeo-Jeong Song ◽  
Dong-Kie Kim ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Hypertrophic Cardiomyopathy ◽  
Paroxysmal Atrial Fibrillation ◽  
Conduction System ◽  
Atrioventricular Conduction ◽  
Wpw Syndrome ◽  
Bypass Tract ◽  
Hypertrophied Myocardium

AbstractHypertrophic cardiomyopathy (HCM) is associated with an increased incidence of Wolff–Parkinson–White (WPW) syndrome and atrial fibrillation. However, a delta-like wide QRS can be observed in the hypertrophied myocardium. When considering the rarity of the paraseptal bypass tract (BT), the normal QRS axis suggests a higher possibility of HCM origin. Otherwise, there is no known electrocardiographic clue indicating a wide QRS differentiation between HCM and WPW syndrome. Moreover, the atriofascicular, nodofascicular/ventricular or fasciculoventricular BT should be differentiated. In this case, atrioventricular conduction system incidental injury revealed a wide QRS origin from the HCM, but this method should be avoided except in some selected cases.

scholarly journals Na/H exchange inhibition in hypertrophied myocardium subjected to cardioplegic arrest: an effective cardioprotective approach

2005 ◽  
Vol 27 (1) ◽  
pp. 111-116 ◽  
Author(s):  
E KEVELAITIS ◽  
A QURESHI ◽  
C MOUAS ◽  
F MAROTTE ◽  
S KEVELAITIENE ◽  
...  
Keyword(s):  
Cardioplegic Arrest ◽  
Hypertrophied Myocardium

scholarly journals Ultrastructural and Stereologic Observations on Hypertrophied Myocardium in Spontaneously Hypertensive Rats

1978 ◽  
Vol 19 (4) ◽  
pp. 579-580
Author(s):  
Kikuko IMAMURA ◽  
Keishiro KAWAMURA ◽  
Tadasu TAKATSU ◽  
Chujiro KASHII
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Hypertrophied Myocardium

scholarly journals The Molecular and Cellular Mechanisms Associated with a Microvascular Inflammation in the Pathogenesis of Heart Failure with Preserved Ejection Fraction

Acta Naturae ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 40-51
Author(s):  
A. G. Ovchinnikov ◽  
T. I. Arefieva ◽  
A. V. Potekhina ◽  
A. Yu. Filatova ◽  
F. T. Ageev ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Severe Disease ◽  
Treatment Options ◽  
Cellular Mechanisms ◽  
Reduced Ejection Fraction ◽  
Hypertrophied Myocardium ◽  
Microvascular Inflammation ◽  
Novel Strategy ◽  
Current Paradigm

Heart failure withpreserved ejection fraction (HFpEF) is a severe disease with an often unfavorable outcome. The prevalence of HFpEF continues to increase, while effective treatment options remain elusive. All the medical strategies used toimprove the outcome in a heart failure with reduced ejection fraction proved ineffective in HFpEF, which was probably due to the different mechanisms ofdevelopment of these two types of heart failure and the diversity of the HFpEF phenotypes. According to the current paradigm of HFpEF development, a chronic mild pro-inflammatory statecauses a coronary microvascular endothelial inflammation, with further myocardial fibrosis and diastolic dysfunction progression. This inflammatory paradigm of HFpEF has been confirmed with someevidence, and suppressing the inflammation may become a novel strategy for treating and managing HFpEF. This review summarizes current concepts about a microvascular inflammation in hypertrophied myocardium and provides a translational perspective of the anti-inflammatory and immunomodulatory approaches in HFpEF.

scholarly journals Structural and metabolic correlates of cell injury in the hypertrophied myocardium during valve replacement

1987 ◽  
Vol 93 (5) ◽  
pp. 741-754 ◽  
Author(s):  
Kenneth G. Warner ◽  
Shukri F. Khuri ◽  
Robert A. Kloner ◽  
Miguel Josa ◽  
Karen M. Dalecki-Chipperfield ◽  
...  
Keyword(s):  
Valve Replacement ◽  
Cell Injury ◽  
Hypertrophied Myocardium

Active force during hypoxia of hypertrophied rabbit right ventricular trabeculae

1987 ◽  
Vol 252 (5) ◽  
pp. H945-H952 ◽  
Author(s):  
M. A. Capeless ◽  
B. B. Hamrell
Keyword(s):  
Stimulus Frequency ◽  
Oxygen Demand ◽  
Peak Stress ◽  
Ringer Solution ◽  
Myocardial Oxygen Demand ◽  
Cross Sectional ◽  
Time To Peak ◽  
Hypertrophied Myocardium ◽  
Pulmonary Artery Constriction ◽  
Ventricular Trabeculae

Hypertrophy is often accompanied by increased myocardial oxygen demand, but any unique effects of hypoxia on contraction in hypertrophy are unknown. Trabeculae from normal [n = 9; 0.119 +/- 0.014 mm2 (means +/- SE) cross-sectional area] and hypertrophied (pulmonary artery constriction; n = 7; 0.108 +/- 0.028 mm2) rabbit right ventricles were subjected to graded hypoxia (Krebs-Ringer solution, 28 degrees C, 1 Hz stimulus frequency). During normoxia, peak active isometric (Pmax) and resting stress (Prest) at optimum length and peak rate of stress development (dP/dt) in hypertrophy were the same as normal and time to peak stress was longer than normal. Time to peak stress and dP/dt decreased with hypoxia, but time to peak stress remained longer than normal in hypertrophy; Prest was unchanged. The ratio of peak active stress (P) during hypoxia to Pmax decreased linearly with superfusate PO2, but the hypertrophy relationship (y = 4.00 X 10(-3) x + 0.084) is the same as normal (y = 3.70 X 10(-3) x + 0.154; p greater than 0.05). Therefore, a normal level of P was preserved in hypertrophied myocardium and prolonged time to peak stress might have been important for that preservation.

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