Diagnosing diabetic cardiomyopathy

2019 ◽  
pp. 13-17
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Myocardial Dysfunction ◽  
Systolic Dysfunction ◽  
Obstructive Coronary Artery Disease ◽  
Left Ventricular ◽  
Concentric Hypertrophy ◽  
Altered Metabolism ◽  
Artery Disease

Diabetic cardiomyopathy reflects the presence of structural or functional abnormalities of the myocardium in an individual with diabetes which are not fully explained by other factors known to cause myocardial dysfunction. Diabetes promotes a range of molecular and cellular changes leading to left ventricular concentric hypertrophy, fibrosis, abnormal perfusion, lipid deposition, altered metabolism, diastolic dysfunction, and later progression to systolic dysfunction. Diagnosis of diabetic cardiomyopathy requires identification of such pathological features whilst at the same time excluding other causes of left ventricular dysfunction. In this article, avail- able modalities which can contribute to a diagnosis of diabetic cardiomyopathy are discussed. In most cases a diagnosis of diabetic cardiomyopathy can be reached by echocardiography or cardiac magnetic resonance imaging to detect structural and functional myocardial changes, with computed tomography coronary angiography being employed to exclude obstructive coronary artery disease which could account for left ventricular dysfunction.

scholarly journals Recurrent Direct Current Cardioversion Induced Takotsubo Cardiomyopathy

2015 ◽  
Vol 3 ◽  
pp. 32
Author(s):  
Athanasios Smyrlis ◽  
Dmitry Yaranov ◽  
Ira Galin ◽  
Shahzad Khan ◽  
Jonathan Alexander
Keyword(s):  
Direct Current ◽  
Takotsubo Cardiomyopathy ◽  
Myocardial Dysfunction ◽  
Systolic Dysfunction ◽  
Obstructive Coronary Artery Disease ◽  
Left Ventricular ◽  
Stress Cardiomyopathy ◽  
Direct Current Cardioversion ◽  
Catecholamine Excess ◽  
Artery Disease

<p>Stress cardiomyopathy (SCM), also called broken heart syndrome and Takotsubo cardiomyopathy is an increasingly reported syndrome generally characterized by transient systolic dysfunction of the apical and or mid segments of the left ventricle that mimics myocardial infarction, in the absence of obstructive coronary artery disease. Typically patients present within a few hours of exposure to physical or emotional stress. However, the mechanism by which these stressors result in myocardial dysfunction is unclear. Proposed factors include catecholamine excess and coronary vasospasm<sup>1</sup>. We present the case of a 61-year-old female who experienced acute pulmonary edema secondary to stress cardiomyopathy, on two occasions immediately after undergoing elective direct current cardioversion (DCCV) for atrial fibrillation (Afib). After an urgent hospitalization for management of acute left ventricular failure, she made a complete clinical and echocardiographic recovery.  The incidence, clinical implications and prognosis of DCCV induced SCM is unknown. Given DCCV for Afib is a common outpatient procedure and DCCV induced SCM can lead to acute clinical deterioration it is important that physicians are vigilant about this newly recognized electrical cardioversion complication.</p>

Atypical Takotsubo Cardiomyopathy with Hypokinetic Left Mid-ventricle and Apical Wall Sparing: A Case Report and Literature Review

2020 ◽  
Vol 16 (3) ◽  
pp. 241-246
Author(s):  
Dipesh Ludhwani ◽  
Belaal Sheikh ◽  
Vasu K Patel ◽  
Khushali Jhaveri ◽  
Mohammad Kizilbash ◽  
...  
Keyword(s):  
Case Report ◽  
Takotsubo Cardiomyopathy ◽  
Systolic Dysfunction ◽  
Obstructive Coronary Artery Disease ◽  
Left Ventricular ◽  
Reduced Ejection Fraction ◽  
Coronary Syndrome ◽  
Normal Left Ventricular ◽  
Artery Disease

Background: Takotsubo Cardiomyopathy (TTC) is an uncommon cause of acute reversible ventricular systolic dysfunction in the absence of obstructive Coronary Artery Disease (CAD). Typically manifesting as apical wall ballooning, TTC can rarely present atypically with apical wall sparing. Case report: A 62-year-old female presented with complaints of chest pain and features mimicking acute coronary syndrome. Coronary angiogram revealed no obstructive CAD and left ventriculogram showed reduced ejection fraction, normal left ventricular apex and hypokinetic mid-ventricles consistent with atypical TTC. The patient was discharged home on heart failure medications and a follow-up transthoracic echocardiogram demonstrated improved left ventricular function with no wall motion abnormality. Conclusion: This case report provides an insight into the diagnosis and management of TTC in the absence of pathognomic features.

scholarly journals Impact of Renin-Angiotensin-Aldosterone System Gene Polymorphisms on Left Ventricular Dysfunction in Coronary Artery Disease Patients

2012 ◽  
Vol 32 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Avshesh Mishra ◽  
Anshika Srivastava ◽  
T. Mittal ◽  
N. Garg ◽  
B. Mittal
Keyword(s):  
Coronary Artery Disease ◽  
Cardiac Output ◽  
Coronary Artery ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
P Value ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Artery Disease

Background: Left ventricular dysfunction (LVD), followed by fall in cardiac output is one of the major complications in some coronary artery disease (CAD) patients. The decreased cardiac output over time leads to activation of the renin-angiotensin-aldosterone system which results in vasoconstriction by influencing salt-water homeostasis. Therefore, the purpose of the present study was to explore the association of single nucleotide polymorphisms (SNPs) in angiotensin I converting enzyme;ACE(rs4340), angiotensin II type1 receptor; AT1 (rs5186) and aldosterone synthase;CYP11B2(rs1799998) with LVD.Methods and results: The present study was carried out in two cohorts. The primary cohort included 308 consecutive patients with angiographically confirmed CAD and 234 healthy controls. Among CAD, 94 with compromised left ventricle ejection fraction (LVEF ≤ 45) were categorized as LVD. The ACE I/D, AT1 A1166C andCYP11B2T-344C polymorphisms were determined by PCR. Our results showed that ACE I/D was significantly associated with CAD but not with LVD. However, AT1 1166C variant was significantly associated with LVD (LVEF ≤ 45) (p value=0.013; OR=3.69), butCYP11B2(rs1799998) was not associated with either CAD or LVD. To validate our results, we performed a replication study in additional 200 cases with similar clinical characteristics and results again confirmed consistent findings (p value=0.020; OR=5.20).Conclusion: AT1 A1166C plays important role in conferring susceptibility of LVD.

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