Angiotensin II and coronary artery disease, congestive heart failure, and sudden cardiac death

1998 ◽  
Vol 93 (0) ◽  
pp. s101-s108 ◽  
Author(s):  
R. Dietz ◽  
R. von Harsdorf ◽  
M. Gross ◽  
J. Krämer ◽  
D. Gulba ◽  
...  
Keyword(s):  
Heart Failure ◽  
Coronary Artery Disease ◽  
Congestive Heart Failure ◽  
Coronary Artery ◽  
Angiotensin Ii ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Artery Disease

scholarly journals Hypoplastic coronary artery disease and hypertension in a child: a case report

2021 ◽  
Author(s):  
Yuji Doi ◽  
Kenji Waki ◽  
Kayo Ogino ◽  
Tomohiro Hayashi
Keyword(s):  
Heart Failure ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Sudden Cardiac Death ◽  
Rare Disease ◽  
Pediatric Patient ◽  
Cardiac Death ◽  
Acute Myocarditis ◽  
Close Observation ◽  
Artery Disease

Abstract Background Hypoplastic coronary artery disease (HCAD) is an extremely rare disease associated with a risk of sudden cardiac death. It is rarely recognized in a live pediatric patient. Case summary We report a case of HCAD in a patient who first presented with vomiting and poor feeding, suggestive of acute heart failure due to cardiomyopathy or acute myocarditis in infancy. Hypertension and signs of ischemia became evident on electrocardiography and scintigraphy after his cardiac function fully recovered, and he was diagnosed with HCAD by angiography performed at the age of eight years. He has remained under close observation with anti-hypertensives, aspirin, and exercise restriction. Discussion Although HCAD is a rare disease, it may not only cause ischemia but may also result in heart failure and sudden cardiac death. It should be considered in any pediatric patient with heart failure. Mid-term follow-up visits might be necessary to detect signs of ischemia in pediatric patients presenting with features of heart failure.

scholarly journals Elevated plasma levels of human urotensin-II immunoreactivity in congestive heart failure

2003 ◽  
Vol 285 (4) ◽  
pp. H1576-H1581 ◽  
Author(s):  
Fraser D. Russell ◽  
Deborah Meyers ◽  
Andrew J. Galbraith ◽  
Nick Bett ◽  
Istvan Toth ◽  
...  
Keyword(s):  
Heart Failure ◽  
Coronary Artery Disease ◽  
Congestive Heart Failure ◽  
Coronary Artery ◽  
Pulmonary Artery ◽  
Femoral Artery ◽  
Aortic Root ◽  
Femoral Vein ◽  
Urotensin Ii ◽  
Artery Disease

Human urotensin-II (hU-II) is the most potent endogenous cardiostimulant identified to date. We therefore determined whether hU-II has a possible pathological role by investigating its levels in patients with congestive heart failure (CHF). Blood samples were obtained from the aortic root, femoral artery, femoral vein, and pulmonary artery from CHF patients undergoing cardiac catheterization and the aortic root from patients undergoing investigative angiography for chest pain who were not in heart failure. Immunoreactive hU-II (hU-II-ir) levels were determined with radioimmunoassay. hU-II-ir was elevated in the aortic root of CHF patients (230.9 ± 68.7 pg/ml, n = 21; P < 0.001) vs. patients with nonfailing hearts (22.7 ± 6.1 pg/ml, n = 18). This increase was attributed to cardiopulmonary production of hU-II-ir because levels were lower in the pulmonary artery (38.2 ± 6.1 pg/ml, n = 21; P < 0.001) than in the aortic root. hU-II-ir was elevated in the aortic root of CHF patients with nonischemic cardiomyopathy (142.1 ± 51.5 pg/ml, n = 10; P < 0.05) vs. patients with nonfailing hearts without coronary artery disease (27.3 ± 12.4 pg/ml, n = 7) and CHF patients with ischemic cardiomyopathy (311.6 ± 120.4 pg/ml, n = 11; P < 0.001) vs. patients with nonfailing hearts and coronary artery disease (19.8 ± 6.6 pg/ml, n = 11). hU-II-ir was significantly higher in the aortic root than in the pulmonary artery and femoral vein, with a nonsignificant trend for higher levels in the aortic root than in the femoral artery. The findings indicated that hU-II-ir is elevated in the aortic root of CHF patients and that hU-II-ir is cleared at least in part from the microcirculation.

P5647Temporal variability of T-wave morphology and risk of sudden cardiac death in patients with coronary artery disease

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
J T Rahola ◽  
A M Kiviniemi ◽  
O H Ukkola ◽  
M P Tulppo ◽  
M J Junttila ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Sudden Cardiac Death ◽  
Spatial Heterogeneity ◽  
Temporal Variability ◽  
Cardiac Death ◽  
T Wave ◽  
Clinical Risk ◽  
Wave Morphology ◽  
Artery Disease

Abstract Background The possible relationship between temporal variability of electrocardiographic spatial heterogeneity of repolarisation and the risk of sudden cardiac death (SCD) in patients with coronary artery disease (CAD) is not completely understood. Purpose To investigate the prognostic value of temporal variability of T-wave spatial heterogeneity in SCD in patients with CAD. Methods The Innovation to reduce Cardiovascular Complications of Diabetes at the Intersection (ARTEMIS) study population consisted of 1,946 patients with angiographically verified CAD. T-wave morphology dispersion (TMD), which estimates the average angle between all reconstruction vector pairs in T-wave loop based on leads I-II and V2-V6, was analysed on beat-to-beat basis from 10 minutes period of the baseline electrocardiographic recording in 1,678 study subjects. The temporal variability of TMD was evaluated by standard deviation of TMD (TMD-SD). Results After on average of 7.4±2.0 years of follow-up, a total of 47 of the 1,678 study subjects (2.8%) had experienced SCD or were resuscitated from sudden cardiac arrest (SCA). TMD-SD was significantly higher in patients who had experienced SCD/SCA compared with those who remained alive (3.64±2.57 vs. 2.65±2.54, p<0.01, respectively), but did not differ significantly between the patients who had experienced non-sudden cardiac death (n=40, 2.4%) and those who remained alive (2.98±2.43 vs. 2.67±2.55, p=0.45, respectively) or between the patients who succumbed to non-cardiac death (n=88, 5,2%) and those who stayed alive (2.74±2.44 vs. 2.67±2.55, p=0.81). After adjustments with relevant clinical risk indicators of SCD/SCA, such as left ventricular ejection fraction, diabetes, left bundle branch block and Canadian Cardiac Society class, TMD-SD still predicted SCD/SCA (HR 1.113, 95% CIs 1.028–1.206, p<0.01). The discrimination and reclassification accuracy increased significantly (p=0.02, p=0.033) and the C-index increased from 0.733 to 0.741 when TMD-SD was added to the clinical risk model of SCD/SCA. The Kaplan-Meier survival curves show proportional probabilities of event-free survival for different modes of death for patients classified according to the optimised TMD-SD cut-off point (Figure). Figure 1 Conclusions Temporal variability of electrocardiographic spatial heterogeneity of repolarisation represented by TMD-SD independently predicts long-term risk of SCD/SCA in patients with CAD. Acknowledgement/Funding Sigrid Juselius Foundation and Finnish Foundation for Cardiovascular Research

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