Idiopathic Dilated Cardiomyopathy

Ss, Coughlin

doi:10.1056/nejm199412083312307

Cited by 850 publications

(491 citation statements)

References 135 publications

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“…The clinical manifestation varies, including dyspnea, exertional intolerance, or a consequence of ventricular dysfunction and heart failure. Growing evidence has directed the clinical significance to the prevention of sudden cardiac death (SCD) in NICM patients, which is usually attributed to ventricular tachyarrhythmias arising from a diseased ventricular substrate 2, 3, 4. Therefore, in the risk stratification of NICM patients, given the potential specific therapies and risk prevention strategies for the nonuniform entities of NICM, the identification of the underlying pathogenesis is of clinical relevance.…”

Section: Introductionmentioning

confidence: 99%

Ventricular arrhythmias in nonischemic cardiomyopathy

Chung

Lin

et al. 2018

Journal of Arrhythmia

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Nonischemic cardiomyopathies (NICMs) are composed of variable disease entities, including primary and secondary cardiomyopathies. Determining the etiology of NICM provides pivotal roles of not only the understanding of the individual pathogenesis, but also the clinical management, such as risk stratification, pharmacological treatment, and intervention therapies. Despite the diverse causes of NICM, these cases mostly require clinical attention owing to progressive myocardial injury, resulting in ventricular dysfunction and heart failure. The interaction between the diseased ventricular substrates and systemic/neurophysiological factors contributes to the cornerstones responsible for ventricular arrhythmogenesis and sudden cardiac death (SCD). Prevention of SCD and diminishing ventricular tachyarrhythmias are the important mainstays for the management of NICM patients. Given the understanding of the abnormal ventricular substrates and advancement of navigation systems, radiofrequency catheter ablation (RFCA) has become an adjunctive or alternative strategy for NICM patients who experience drug‐refractory ventricular tachycardias (VTs). Successful ablation can frequently be achieved at the expense of an epicardial intervention. A recent study has proven the survival benefits for NICM patients who are free from recurrent VTs after a successful RFCA, regardless of the New York Heart Association (NYHA) functional class status or left ventricular ejection fraction. Additionally, recent evidence has highlighted the better delineation of a diseased myocardium through the incorporation of cardiovascular magnetic resonance imaging (CMRI) and 3D mapping systems, which can facilitate the identification of critical ventricular arrhythmogenic substrates in NICM patients.

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Section: Introductionmentioning

confidence: 99%

Ventricular arrhythmias in nonischemic cardiomyopathy

Chung

Lin

et al. 2018

Journal of Arrhythmia

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“…In 2013, CMS enforced the “2 midnights” rule, which meant that a patient had to stay at least 2 consecutive midnights at the hospital to count as an inpatient admission; otherwise, it would be counted as an admission OBS 4. This had significant implications on both hospitals and patients.…”

Section: Introductionmentioning

confidence: 99%

Outcomes of Heart Failure Admissions Under Observation Versus Short Inpatient Stay

Masri

Althouse

McKibben

et al. 2018

JAHA

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BackgroundPatients with heart failure (HF) are admitted either under observation (OBS) or inpatient stays; however, there is little data on whether this designation reflects the clinical status of a patient, with significant logistical and financial implications. We sought to compare the outcomes of patients with HF admitted OBS versus inpatient stay (≤2 days; INPT).Methods and ResultsFrom January 1, 2008 to September 30, 2015, our multisite health system saw 21 339 unique patients totaling 52 493 hospital admissions with a primary diagnosis of HF. Patients were excluded if they underwent cardiac surgery (n=611), heart transplantation (n=187), or left ventricular assist device insertion (n=198), or if they died during hospitalization (n=1839). Of the remaining 50 654 discharges, 2 groups were identified: INPT group and OBS group. Outcomes were HF readmission, all‐cause readmission, and all‐cause mortality within 1 year of discharge. Hazard ratios were computed using the Andersen‐Gill method in the Cox proportional‐hazards model. A total of 8709 admissions (17%) occurred in the INPT group and 2648 admissions (5%) occurred in the OBS group. HF readmission rate at 1 year was 55.3% in INPT versus 66.5% in OBS (hazard ratio, 0.75; 95% confidence interval, 0.71–0.80; P<0.01). All‐cause readmission rate at 1 year was 70.7% in INPT versus 82.5% in OBS (hazard ratio, 0.74; 95% confidence interval, 0.70–0.78; P<0.01). All‐cause mortality at 1 year occurred in 25.2% of INPT versus 24.2% of OBS (hazard ratio, 1.03; 95% confidence interval, 0.95–1.12; P=0.46).Conclusions HF admissions designated INPTs were associated with lower readmission rates and equivalent mortality to those designated OBS.

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“…Mutations in genes encoding myocyte structural proteins are found in about 30-40% of DCM, but the etiology of the remaining 60-70% of cases is poorly understood [1][2][3]. Advances in the field of immunology have shed light on the close relationship between immunological disturbances and the progression of heart failure [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Autoimmunity against M₂ muscarinic acetylcholine receptor induces myocarditis and leads to a dilated cardiomyopathy‐like phenotype

et al. 2012

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Patients with dilated cardiomyopathy (DCM) often have autoantibodies against cardiac antigens including the M 2 muscarinic acetylcholine receptor (M 2 R). To elucidate the role of autoimmunity against M 2 R in disease development, we induced an immune response against M 2 R by adoptive transfer into Rag2 -/-mice of splenocytes from M 2 R -/-mice immunized with a recombinant M 2 R protein. T lymphocytes transiently infiltrated the heart in recipient mice followed by morphological changes in cardiomyocytes. These mice produced IgG antibodies against M 2 R, which bound to cardiomyocytes in vivo and decreased the amplitude of calcium signals in isolated rat cardiomyocytes in vitro. Recipient mice showed increased heart weights associated with increased intraventricular diameter, decreased systolic function, and increased action potential duration, which are characteristics of DCM. Our results suggest that myocarditis and DCM associated with the presence of anti-M 2 R antibodies are autoimmune diseases with a risk of progressing to the terminal stage. Our mouse model will be useful in the analysis of the molecular mechanisms of disease progression and the development of new therapies for DCM. Keywords IntroductionDilated cardiomyopathy (DCM) causes severe heart failure in young adults including occasional sudden cardiac death. Mutations in genes encoding myocyte structural proteins are found in about 30-40% of DCM, but the etiology of the remaining 60-70% of cases is poorly understood [1][2][3]. Advances in the field of immunology have shed light on the close relationship between immunological disturbances and the progression of heart failure [4][5][6][7]. Adenovirus or enterovirus-specific RNA sequences are often detected in the myocardium of patients with DCM and myocarditis [7][8][9]. Myocardial-reactive antibodies such as those against β 1 adrenergic receptor (β 1 AR), M 2 muscarinic acetylcholine receptor (M 2 R), and cardiac myosin have also been observed in the sera of these patients [10][11][12][13][14]. As a result, it has been hypothesized that prolonged immunological abnormalities after myocarditis, presumably induced by a subclinical viral infection or autoimmunity, could lead to DCM [5,6]. Evidence supporting this hypothesis has accumulated through clinical and experimental studies [15][16][17].For example, immunization of animals with peptides derived from proteins expressed in cardiomyocytes such as β 1 AR [16,17] or cardiac myosin [15] or the transfer of antibodies against cardiac antigens mimics the prolonged immune abnormalities observed after acute myocarditis [18,19]. However, the progression from myocarditis to DCM has not been investigated in detail. The causes of the initial myocardial damage and subsequent cardiac dysfunction along with the subsequent role of autoimmunity in DCM are still unclear.The pathophysiological role of autoantibodies in disease progression has been established in only some autoimmune diseases such as pemphigus vulgaris (PV), involving anti-desmoglein 3 (Dsg3) antibodi...

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Idiopathic Dilated Cardiomyopathy

Cited by 850 publications

References 135 publications

Ventricular arrhythmias in nonischemic cardiomyopathy

Ventricular arrhythmias in nonischemic cardiomyopathy

Outcomes of Heart Failure Admissions Under Observation Versus Short Inpatient Stay

Autoimmunity against M₂ muscarinic acetylcholine receptor induces myocarditis and leads to a dilated cardiomyopathy‐like phenotype

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Idiopathic Dilated Cardiomyopathy

Cited by 850 publications

References 135 publications

Ventricular arrhythmias in nonischemic cardiomyopathy

Ventricular arrhythmias in nonischemic cardiomyopathy

Outcomes of Heart Failure Admissions Under Observation Versus Short Inpatient Stay

Autoimmunity against M2 muscarinic acetylcholine receptor induces myocarditis and leads to a dilated cardiomyopathy‐like phenotype

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Autoimmunity against M₂ muscarinic acetylcholine receptor induces myocarditis and leads to a dilated cardiomyopathy‐like phenotype