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.

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

scholarly journals Exposure to diesel exhaust particulates induces cardiac dysfunction and remodeling

2013 ◽  
Vol 115 (7) ◽  
pp. 1099-1106 ◽  
Author(s):  
Jessica M. Bradley ◽  
Kipp A. Cryar ◽  
Milad C. El Hajj ◽  
Elia C. El Hajj ◽  
Jason D. Gardner
Keyword(s):  
Diesel Exhaust ◽  
Ventricular Remodeling ◽  
Diastolic Pressure ◽  
Hypoxia Inducible Factor ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Internal Diameter ◽  
Ventricular Dilation ◽  
Hypoxia Inducible Factor 1Α ◽  
Left Ventricular Dilation

Chronic exposure to diesel exhaust particulates (DEP) increases the risk of cardiovascular disease in urban residents, predisposing them to the development of several cardiovascular stresses, including myocardial infarctions, arrhythmias, thrombosis, and heart failure. DEP contain a high level of polycyclic aromatic hydrocarbons, which activate the aryl hydrocarbon receptor (AHR). We hypothesize that exposure to DEP elicits ventricular remodeling through the activation of the AHR pathway, leading to ventricular dilation and dysfunction. Male Sprague-Dawley rats were exposed by nose-only nebulization to DEP (SRM 2975, 0.2 mg/ml) or vehicle for 20 min/day × 5 wk. DEP exposure resulted in eccentric left ventricular dilation (8% increased left ventricular internal diameter at diastole and 23% decreased left ventricular posterior wall thickness at diastole vs. vehicle), as shown by echocardiograph assessment. Histological analysis using Picrosirius red staining revealed that DEP reduced cardiac interstitial collagen (23% decrease vs. vehicle). Further assessment of cardiac function using a pressure-volume catheter indicated impaired diastolic function (85% increased end-diastolic pressure and 19% decreased Tau vs. vehicle) and contractility (57 and 48% decreased end-systolic pressure-volume relationship and maximum change in pressure over time vs. end-diastolic volume compared with vehicle, respectively) in the DEP-exposed animals. Exposure to DEP significantly increased cardiac expression of AHR (19% increase vs. vehicle). In addition, DEP significantly decreased the cardiac expression of hypoxia inducible factor-1α, the competitive pathway to the AHR, and vascular endothelial growth factor, a downstream mediator of hypoxia inducible factor-1α (26 and 47% decrease vs. vehicle, respectively). These findings indicate that exposure to DEP induced left ventricular dilation by loss of collagen through an AHR-dependent mechanism.

Electrocardiographic and echocardiographic evaluation of a large cohort of peri-pubertal soccer players during pre-participation screening

2019 ◽  
Vol 26 (13) ◽  
pp. 1444-1455 ◽  
Author(s):  
Leonardo Calò ◽  
Annamaria Martino ◽  
Eliana Tranchita ◽  
Fabio Sperandii ◽  
Emanuele Guerra ◽  
...  
Keyword(s):  
Cardiovascular Events ◽  
Ventricular Hypertrophy ◽  
Young Male ◽  
Left Ventricular ◽  
Soccer Players ◽  
Young Athletes ◽  
Ventricular Dilation ◽  
Cardiac Abnormalities ◽  
Major Cardiovascular Events ◽  
Left Ventricular Dilation

Background The early diagnosis of cardiac abnormalities in young athletes may be helpful not only to identify subjects potentially at risk of sudden cardiac death but also to prevent stress-related cardiac dysfunction and cardiovascular events during the life of these subjects. The aim of our study was to investigate the prevalence of cardiac abnormalities in a population of young male soccer players undergoing pre-participation screening through electrocardiogram and trans-thoracic echocardiography. Methods All consecutive male football players undergoing pre-participation screening comprehensive of medical history, physical examination, 12-lead electrocardiogram and trans-thoracic echocardiography at the FMSI Sport Medicine Institute in Rome between January 2008–March 2009 were enrolled in the study. Results Overall, 2261 consecutive young athletes aged 12.4 ± 2.6 years were evaluated. Training-unrelated electrocardiogram abnormalities were observed in 65 (2.9%) athletes. Abnormal trans-thoracic echocardiography was observed in 102 athletes (4.5%), including two cases of hypertrophic cardiomyopathy, eight of mild left ventricular hypertrophy, six of mild left ventricular dilation and 17 of bicuspid aortic valve. An abnormal electrocardiogram was associated with anomalous trans-thoracic echocardiography in 11/65 (16.9%) cases. All athletes requiring sport disqualification were identified by electrocardiogram. Notably, among 2216 athletes with a normal electrocardiogram, 91 had abnormal trans-thoracic echocardiography, including six cases of left ventricular dilation and six of ventricular hypertrophy. Conclusions In a wide population of peri-pubertal male athletes, evaluation of the electrocardiogram identified all cardiac diseases requiring sport disqualification. Trans-thoracic echocardiography alone allowed the identification of cardiac abnormalities potentially leading to cardiomyopathies or major cardiovascular events over time.

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.

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