True left ventricular aneurysm and healed myocardial infarction

Cabin, Henry S.; Roberts, William C.

doi:10.1016/0002-9149(80)90425-7

Cited by 81 publications

(5 citation statements)

References 19 publications

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“…Several studies have shown that LVA is mostly associated with the single-vessel disease, [2,21] others had suggested that the multivessel disease was an independent predictor in the development of LVA. [21,22] Our finding is consistent with the findings that single-vessel disease is the most prevalent angiographic finding in patients that developed an aneurysm after anterior MI. [2,21] In patients with the multivessel disease, the occurrence of less aneurysm formation may be related to the diffusely impaired LV function, so the demarcation of the infarct area from the noninfarct area may not have been well defined.…”

Section: Discussionsupporting

confidence: 91%

Impaired renal function and abnormal level of ferritin are independent risk factors of left ventricular aneurysm after acute myocardial infarction

Feng¹,

Wang

Chen³

et al. 2018

Medicine

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This study was performed to determine the prognostic value of glomerular filtration rate (GFR) and ferritin compromised in left ventricular aneurysm (LVA) patients who suffered acute myocardial infarction (AMI) beforehand.A hospital-based case-control study was conducted in the Department of Cardiology, First Affiliated Hospital, Zhejiang University in 2013 and 2014. Patients were divided into 3 groups according to kidney function and ferritin level. Observation outcomes include age, sex, C-reaction protein (CRP), medical history including major risk factors for CAD, ferritin and GFR, previous angina, time between MI and coronary angiography or time to rescue (TTR), and prior treatment.Around 60 patients were included in the case group (AMI with LVA) and 133 matched patients (AMI without LVA) in the control group. The prevalence of single-vessel disease (odd ratio [OR] = 2.490; 95% confidential interval [95% CI] = 1.376-4.506; P = .002), total LAD occlusion (OR = 1.897; 95% CI = 1.024-3.515; P = .041), absence of previous angina (OR = 1.930; 95% CI = 1.035-3.600; P = .037), time between myocardial infraction (MI) and coronary angiography more than 12 h (OR = 1.970; 95% CI = 1.044-3.719; P = .035), GFR less than 60 mL/min (OR = 2.933; 95% CI = 1.564-5.503; P = .001), and ferritin levels (P = .0003) were all higher in the aneurysm group compared with those in the control group. After adjustments for other variables, single-vessel disease (OR = 1.211; 95% CI = 1.080-1.342; P = .02), GFR lower than 60 mL/min (OR = 1.651; 95% CI = 1.250-2.172; P = .013), and high or low levels of ferritin (OR = 1.151; 95% CI = 1.050-1.252; P = .042) remained the independent determinants of LVA formation after AMI.Decreased GFR and abnormal ferritin levels are independent risk factors of LVA formation after AMI.

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Section: Discussionsupporting

confidence: 91%

Impaired renal function and abnormal level of ferritin are independent risk factors of left ventricular aneurysm after acute myocardial infarction

Feng¹,

Wang

Chen³

et al. 2018

Medicine

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“…In patients with coronary artery disease and animal models of myocardial infarction, the pathological process to HF leads to extensive cardiac myocyte death and results in ventricular scar regions consisting of dense fibrosis with collagen and fibrocytes (Cabin and Roberts, 1980; de Bakker et al, 1993; Lo and Hsia, 2008; Soejima et al, 2002; Stevenson, 2009). Light microscopy findings in humans demonstrated that the distribution of connexin 43 gap junctions in the border zone of the infarcted human heart are organized into transverse (side-to-side) connections but not a normal longitudinal connections (Peters et al, 1997; Peters and Wit, 1998; Peters and Wit, 2000).…”

Section: Substrates For Ventricular Arrhythmias In Hfmentioning

confidence: 99%

Substrates and potential therapeutics of ventricular arrhythmias in heart failure

Zhang

Wadman

et al. 2018

European Journal of Pharmacology

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Heart failure (HF) is a clinical syndrome characterized by ventricular contractile dysfunction. About 50% of death in patients with HF are due to fetal ventricular arrhythmias including ventricular tachycardia and ventricular fibrillation. Understanding ventricular arrhythmic substrates and discovering effective antiarrhythmic interventions are extremely important for improving the prognosis of patients with HF and reducing its mortality. In this review, we discussed ventricular arrhythmic substrates and current clinical therapeutics for ventricular arrhythmias in HF. Base on the fact that classic antiarrhythmic drugs have the limited efficacy, side effects, and proarrhythmic potentials, we also updated some therapeutic strategies for the development of potential new antiarrhythmic interventions for patients with HF.

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“…Congestive heart failure is frequent, being the major cause of death. 11 The mortality rate of patients of both sexes, aged at least 70 years, who develop CHF after myocardial infarction and have an abnormal left ventricular ejection fraction, varies from 41% to 92%, respectively, from the first to the fifth post-infarction year. 12 In the case here discussed, the complication cited contributed to CHF, morphologically identified as anasarca, chronic passive congestion of the lungs, liver and spleen, low cardiac output and cardiac cachexia, determining the patient’s unfavorable outcome.…”

Section: Commentsmentioning

confidence: 99%