Sudden, unexpected death in cardiac transplant recipients: an autopsy study

Chantranuwat, Chavit; Blakey, John; Kobashigawa, Jon A.; Moriguchi, J.; Laks, Hillel; Vassilakis, Maria Espejo; Fishbein, Michael C.

doi:10.1016/s1053-2498(03)00295-x

Cited by 73 publications

(58 citation statements)

References 17 publications

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“…Those results support the close relationship between left ventricular function and SNS activity in patients with ventricular tachyarrhythmia. On the other hand, patients who underwent heart transplantation and had denervated hearts did not show severe left ventricular dysfunction, but about 10% of the patients experienced sudden cardiac death, presumably due to arrhythmia (29), suggesting a direct effect of SNS abnormality (30)(31)(32). In the present study, SNS abnormality increased the occurrence of recurrent ventricular arrhythmia independent of left ventricular dysfunction or structural heart disease.…”

Section: Sns Abnormality In Patients With a History Of Ventricular Arcontrasting

confidence: 39%

The Significance of Cardiac Sympathetic Nervous System Abnormality in the Long-Term Prognosis of Patients with a History of Ventricular Tachyarrhythmia

Akutsu¹,

Kaneko²,

Kodama³

et al. 2008

J Nucl Med

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Severe left ventricular dysfunction or cardiac sympathetic nervous system (SNS) abnormality predicts cardiac death in various heart diseases, including arrhythmogenic disorders. However, it is not clear whether SNS abnormality predicts sudden cardiac death during long-term follow-up in patients with a history of ventricular tachyarrhythmia. We hypothesized that SNS abnormality would be associated with recurrent ventricular arrhythmic events. Methods: 123 I-metaiodobenzylguanidine (MIBG) scintigraphy was performed on 86 patients (mean age 6 SD, 46 6 19 y, 65.1% men) with a history of ventricular tachycardia or fibrillation. 123 I-MIBG (111 MBq) was intravenously administered under resting conditions, and planar images were obtained 15 min and 4 h later (anterior view for 6 min; 512 · 512 matrices; zoom ratio, 1.0). SNS activity was assessed using the heart-to-mediastinum ratio on delayed imaging. Results: During about 11 y of followup (mean 6 SD, 5.2 6 3.7 y), 3 patients (3.5%) had sudden cardiac death and 21 patients (24.4%) had sustained ventricular tachyarrhythmic events. SNS abnormality, defined as a heart-tomediastinum ratio of less than 2.8, and left ventricular dysfunction, defined as a left ventricular ejection fraction of less than 50%, were associated with sudden cardiac death or recurrent ventricular tachyarrhythmic events (18/40 patients [45%] with SNS abnormality, vs. 6/46 patients [13%] without, P 5 0.004; 9/15 patients [60%] with left ventricular dysfunction, vs. 15/71 patients [21.1%] without, P 5 0.008). After adjustment for potential confounding variables such as age, sex, coronary risk factors, medication use, history of structural heart disease, and left ventricular function, SNS abnormality was a powerful predictor of recurrent arrhythmic events, with a hazard ratio of 3.6 [95% confidence interval, 1.4-9.2, P 5 0.007]). Further, SNS abnormality had incremental and additive prognostic power in combination with left ventricular dysfunction, with an adjusted hazard ratio of 4.4 [95% confidence interval, 1.9-9.9, P , 0.0001]). Conclusion: SNS abnormality predicted recurrent ventricular tachyarrhythmic events during long-term follow-up. 123 I-MIBG scintigraphic evaluations for SNS abnormality may be an option for screening patients at high risk for sudden cardiac death.

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Section: Sns Abnormality In Patients With a History Of Ventricular Arcontrasting

confidence: 39%

The Significance of Cardiac Sympathetic Nervous System Abnormality in the Long-Term Prognosis of Patients with a History of Ventricular Tachyarrhythmia

Akutsu¹,

Kaneko²,

Kodama³

et al. 2008

J Nucl Med

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“…The greatest literature impact on the QE comes from the 1990s, when its inflammatory composition and potential mechanism were studied. Some authors connected the QE with cyclosporine therapy [5], the QE being thought to be a kind of ACR [8,9]. Most of these findings are no longer sustained.…”

Section: Discussionmentioning

confidence: 99%

“…Further studies [6,7] did not prove that hypothesis as the lesion had been found in EMBs of patients treated with different kinds of immunomodulators. Other authors [8,9] believed that the QE was a kind of low-grade cellular rejection (ACR), specially type B. The potential mechanism was separation of inflammatory infiltrates from the endocardium.…”

Section: Introductionmentioning

confidence: 99%

Prevalence of the Quilty effect in endomyocardial biopsy of patients after heart transplantation – from cellular rejection to antibody-mediated rejection?

Szymańska¹,

Grajkowska²,

Sobieszczańska−Małek³

et al. 2016

pjp

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The significance of the Quilty effect (QE) is not fully understood. It was once proposed to be related to acute cellular rejection (ACR). We aim to assess the relation between QE prevalence and antibody-mediated rejection (AMR). One thousand three hundred and fifty endomyocardial biopsies (EMBs) from 212 patients who underwent heart transplantation in the years 2001-2013 and survived a period of 30 days after the operation were diagnosed. In all EMBs routine HE staining and additional immunohistochemical staining with polyclonal antibody against C4d were performed. Microscopic findings were classified according to the new ISHLT 2013 criteria. Patients were separated into two groups: group 1 included those with at least one pAMR1 I+ and/or pAMR2 EMB (n = 16), and group 2 included the rest of the patients (n = 196). Presence of QE with distinguishing subtypes A and B (according to the first ISHLT 1990 criteria) was assessed. One hundred and twenty one EMBs from group 1 and 1229 EMBs from group 2 were diagnosed. Quilty effect type A was found in 16 (13.2%) EMBs in group 1 and in 96 (7.8%) EMBs in group 2, p < 0.001. Quilty effect type B was diagnosed in 52 (43%) EMBs in group 1 and in 245 (20%) EMBs in group 2, p < 0.001. The QE was not present in 53 (43.8%) EMBs in group 1 and in 888 (72.2%) EMBs in group 2, p < 0.001. The relation between QE prevalence and AMR is possible as the QE is present statistically more often in EMBs of patients with C4d capillary depositions.

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“…It affects epicardial, intramural arteries, and veins and causes diffuse luminal narrowing which could lead to myocardial infarction (MI) and graft dysfunction [11]. CAV can be indolent or may lead to clinical sequelae such as MI, decreased exercise capacity, heart failure, arrhythmia, and sudden cardiac death [12][13][14]. Clinical presentation is usually delayed as patients usually do not experience angina due to denervated status of the transplant heart and can have silent MI.…”

Section: Introductionmentioning

confidence: 99%

Cardiac Allograft Vasculopathy: A Review of Risk Factors and Pathogenesis

Munagala¹,

Phancao²

2018

obm.transplant

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Heart transplant remains the gold standard therapy for patients with end stage heart disease and offers improved survival and quality of life. Significant progress has been achieved in improving one-year mortality after heart transplantation. Nonetheless, longterm graft survival has not changed significantly over the past few decades. Long term survival of heart transplant recipients is limited by chronic rejection, cardiac allograft vasculopathy (CAV), and malignancy. CAV is a major contributor for graft failure and mortality after the first year of in heart transplant recipients. CAV is a proliferative vasculopathy characterized by diffuse myointimal hyperplasia and progressive narrowing of the graft vessels. Both immune dependent and independent factors have been shown to contribute to the pathogenesis of CAV. Understanding these risk factors is essential in developing preventative and therapeutic strategies. Angiography with Intravascular ultrasound has become the key diagnostic tool in the early detection of CAV as well as prognostication. Echocardiographic assessment of allograft function in conjunction with coronary angiographic findings are used in assessing the severity of CAV. Adjustment of immunosuppression and statins remain the initial steps in the management of CAV. Retransplantation is the definitive treatment for severe CAV, however, the paucity of organs along with increased mortality associated with retransplantation makes it a less desirable option. Remarkable progress has been achieved in the understanding of pathogenesis, risk factors for CAV and plaque morphology. Nevertheless, significant knowledge gaps persist in scientific understanding of risk factors, pathogenesis, prevention and treatment of CAV. Further research is warranted to fill these gaps, develop diagnostic modalities to facilitate early detection of CAV, and management strategies to Improve graft tolerance and immune modulation. This review focuses on summarizing the pathogenesis and risk factors for CAV.

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Sudden, unexpected death in cardiac transplant recipients: an autopsy study

Cited by 73 publications

References 17 publications

The Significance of Cardiac Sympathetic Nervous System Abnormality in the Long-Term Prognosis of Patients with a History of Ventricular Tachyarrhythmia

The Significance of Cardiac Sympathetic Nervous System Abnormality in the Long-Term Prognosis of Patients with a History of Ventricular Tachyarrhythmia

Prevalence of the Quilty effect in endomyocardial biopsy of patients after heart transplantation – from cellular rejection to antibody-mediated rejection?

Cardiac Allograft Vasculopathy: A Review of Risk Factors and Pathogenesis

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