Arrhythmogenic effect of ventriculography in patients with left ventricular dilation and/or hypertrophy

1998 ◽  
Vol 95 (4) ◽  
pp. 453 ◽  
Author(s):  
Abdulhalim S. SERAFI ◽  
Stephen J. EVANS ◽  
John V. JONES
Keyword(s):  
Left Ventricular ◽  
Ventricular Dilation ◽  
Arrhythmogenic Effect ◽  
Left Ventricular Dilation

Arrhythmogenic effect of ventriculography in patients with left ventricular dilation and/or hypertrophy

1998 ◽  
Vol 95 (4) ◽  
pp. 453-458
Author(s):  
Abdulhalim S. SERAFI ◽  
Stephen J. EVANS ◽  
John V. JONES
Keyword(s):  
Contrast Medium ◽  
Ventricular Hypertrophy ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Complex Interplay ◽  
Ventricular Dilation ◽  
Arrhythmogenic Effect ◽  
Left Ventricular Dilation ◽  
Acute Injection ◽  
Ventricular Dimension

1.This study examined the effect of an acute injection of contrast medium on generation of arrhythmias in diseased hearts in man. 2.Subjects were 100 patients in sinus rhythm undergoing cardiac catheterization in whom good quality echocardiograms could be obtained. The subjects comprised 78 males and 22 females aged 37–83 years. 3.Arrhythmia induced by left ventricular angiography ranged from nil to brief bursts of ventricular tachycardia. There was a strongly positive relationship between left ventricular internal dimension in diastole (LVIDd) and induced arrhythmia. Out of 26 patients, 25 developed arrhythmia when LVIDd ⩾ 5 ;cm (96%), but only 24 out of 74 patients developed arrhythmia when LVIDd < 5 ;cm (32%) (P< 0.001). In non-dilated hearts where K+ < 4.0 ;mmol/l, arrhythmia developed in 100% (10 out of 10) of those with left ventricular hypertrophy (LVH), but in only 40% (8 out of 20) without LVH (P< 0.005). Where K+ ⩾ 4.0 ;mmol/l, no arrhythmia occurred in patients with LVH but was present in 52% (31 out of 60) of patients without LVH (P< 0.005). There were no relationships with age, end-diastolic pressure, blood pressure, ischaemic heart disease or sex of patient. 4.These data support the view that acute injection of contrast medium in humans induces arrhythmias dependent upon the underlying state of the heart, with potentially complex interplay between left ventricular dimension, hypertrophy and potassium status, supporting similar observations in experimental animals.

scholarly journals Exaggerated Left Ventricular Dilation and Reduced Collagen Deposition After Myocardial Infarction in Mice Lacking Osteopontin

2001 ◽  
Vol 88 (10) ◽  
pp. 1080-1087 ◽  
Author(s):  
Nathan A. Trueblood ◽  
Zhonglin Xie ◽  
Catherine Communal ◽  
Flora Sam ◽  
Soeun Ngoy ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular ◽  
Collagen Deposition ◽  
Ventricular Dilation ◽  
Left Ventricular Dilation

Post-stress end-systolic left ventricular dilation: a marker of endocardial post-ischemic stunning

2001 ◽  
Vol 22 (6) ◽  
pp. 685-693 ◽  
Author(s):  
A. BESTETTI ◽  
C. DI LEO ◽  
A. ALESSI ◽  
A. TRIULZI ◽  
L. TAGLIABUE ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Ventricular Dilation ◽  
Left Ventricular Dilation ◽  
Post Stress

scholarly journals Collateral channels that develop after an acute myocardial infarction prevent subsequent left ventricular dilation

1996 ◽  
Vol 27 (5) ◽  
pp. 1133-1139 ◽  
Author(s):  
Kazuhisa Kodama ◽  
Hideo Kusuoka ◽  
Akihiko Sakai ◽  
Takayoshi Adachi ◽  
Shinji Hasegawa ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Left Ventricular ◽  
Ventricular Dilation ◽  
Left Ventricular Dilation

Co-morbidity (HFrEF and HFpEF): hypertension

ESC CardioMed ◽  
2018 ◽  
pp. 1808-1812
Author(s):  
Francesco Paneni ◽  
Massimo Volpe
Keyword(s):  
Blood Pressure ◽  
Ejection Fraction ◽  
Left Ventricular ◽  
Ventricular Dilation ◽  
Hypertensive Patients ◽  
Reduced Ejection Fraction ◽  
Concentric Hypertrophy ◽  
Drug Classes ◽  
Left Ventricular Dilation ◽  
Eccentric Hypertrophy

Hypertensive heart disease is a major cause of heart failure (HF) and mortality. Hypertension precedes HF occurrence in 75% of cases, and carries a sixfold increase in HF risk as compared to non-hypertensive individuals. Most importantly, a minority of patients survive 5 years after the onset of hypertensive HF. In hypertensive patients, the heart may present different patterns of adaptive remodelling: concentric remodelling, concentric hypertrophy, and eccentric hypertrophy. Although most hypertensive patients are at high risk of developing concentric hypertrophy, a growing proportion of subjects display a concentric-to-eccentric progression eventually leading to left ventricular dilation and systolic dysfunction. Several factors including myocardial ischaemia, ethnicity, genetic background, history of diabetes, and blood pressure pattern may significantly influence the pathway from hypertension to left ventricular dilation. Patients with a concentric hypertrophy usually develop HF with preserved ejection fraction (HFpEF), whereas those with an eccentric (dilated) phenotype develop HF with reduced ejection fraction (HFrEF). Lowering blood pressure has a striking effect in reducing the risk of HF. Although available antihypertensive drugs are all successful in lowering blood pressure, angiotensin-converting enzyme inhibitors, angiotensin receptor blocker (ARBs), and diuretics are more effective than other drug classes in preventing HF. The combination of the neprilysin inhibitor sacubitril with the ARB valsartan (LCZ696) has recently been shown to be highly effective in reducing HF-related outcomes in hypertensive subjects. An individualized treatment scheme taking into account blood pressure levels, type of HF (HFpEF or HFrEF), and relevant co-morbidities (i.e. renal disease, diabetes) is currently the best approach to improve morbidity and mortality in hypertensive patients with HF.

Co-morbidity (HFrEF and HFpEF): hypertension

2019 ◽  
Author(s):  
Francesco Paneni ◽  
Massimo Volpe
Keyword(s):  
Blood Pressure ◽  
Ejection Fraction ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Ventricular Dilation ◽  
Hypertensive Patients ◽  
Concentric Hypertrophy ◽  
Left Ventricular Dilation ◽  
Neprilysin Inhibitor ◽  
Co Morbidity

Hypertensive heart disease is a major cause of heart failure (HF) and mortality. Hypertension precedes HF occurrence in 75% of cases, and carries a sixfold increase in HF risk as compared to non-hypertensive individuals. Most importantly, a minority of patients survive 5 years after the onset of hypertensive HF. In hypertensive patients, the heart may present different patterns of adaptive remodelling: concentric remodelling, concentric hypertrophy, and eccentric hypertrophy. Although most hypertensive patients are at high risk of developing concentric hypertrophy, a growing proportion of subjects display a concentric-to-eccentric progression eventually leading to left ventricular dilation and systolic dysfunction. Several factors including myocardial ischaemia, ethnicity, genetic background, history of diabetes, and blood pressure pattern may significantly influence the pathway from hypertension to left ventricular dilation. Patients with a concentric hypertrophy usually develop HF with preserved ejection fraction (HFpEF), whereas those with an eccentric (dilated) phenotype develop HF with reduced ejection fraction (HFrEF). Lowering blood pressure has a striking effect in reducing the risk of HF. Although available antihypertensive drugs are all successful in lowering blood pressure, angiotensin-converting enzyme inhibitors, angiotensin receptor blocker (ARBs), and diuretics are more effective than other drug classes in preventing HF. The combination of the neprilysin inhibitor sacubitril with the ARB valsartan (LCZ696) has recently been shown to be highly effective in reducing HF-related outcomes in hypertensive subjects. An individualized treatment scheme taking into account blood pressure levels, type of HF (HFpEF or HFrEF), and relevant co-morbidities (i.e. renal disease, diabetes) is currently the best approach to improve morbidity and mortality in hypertensive patients with HF.

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