BackgroundHypertrophic cardiomyopathy (HCM) is characterized by myocyte hypertrophy, disarray, fibrosis, and increased risk for ventricular arrhythmias. Increased QT dispersion has been reported in patients with HCM, but the underlying mechanisms have not been completely elucidated. In this study, we examined the relationship between diffuse interstitial fibrosis, replacement fibrosis, QTc dispersion and ventricular arrhythmias in patients with HCM. We hypothesized that fibrosis would slow impulse propagation and increase dispersion of ventricular repolarization, resulting in increased QTc dispersion on surface electrocardiogram (ECG) and ventricular arrhythmias.MethodsECG and cardiac magnetic resonance (CMR) image analyses were performed retrospectively in 112 patients with a clinical diagnosis of HCM. Replacement fibrosis was assessed by measuring late gadolinium (Gd) enhancement (LGE), using a semi-automated threshold technique. Diffuse interstitial fibrosis was assessed by measuring T1 relaxation times after Gd administration, using the Look–Locker sequence. QTc dispersion was measured digitally in the septal/anterior (V1–V4), inferior (II, III, and aVF), and lateral (I, aVL, V5, and V6) lead groups on surface ECG.ResultsAll patients had evidence of asymmetric septal hypertrophy. LGE was evident in 70 (63%) patients; the median T1 relaxation time was 411±38 ms. An inverse correlation was observed between T1 relaxation time and QTc dispersion in leads V1–V4 (p<0.001). Patients with HCM who developed sustained ventricular tachycardia had slightly higher probability of increased QTc dispersion in leads V1–V4 (odds ratio, 1.011 [1.004–1.0178, p=0.003). We found no correlation between presence and percentage of LGE and QTc dispersion.ConclusionDiffuse interstitial fibrosis is associated with increased dispersion of ventricular repolarization in leads, reflecting electrical activity in the hypertrophied septum. Interstitial fibrosis combined with ion channel/gap junction remodeling in the septum could lead to inhomogeneity of ventricular refractoriness, resulting in increased QTc dispersion in leads V1–V4.
The exercise heart rate (HR) profile and its relationship to cardiac function and arrhythmias was investigated in patients with hypertrophic cardiomyopathy (HC). Chronotropic response (CR) and heart rate recovery (HRR) were computed during and after treadmill exercise testing in 273 HC patients and 95 age-matched healthy controls. HC patients had higher prevalence of chronotropic incompetence and lower HRR1–5min compared to controls. Exercise capacity, diastolic function (assessed by E/e' and left atrial volume index were associated with HRR1min and CR in HC. Septal myectomy was associated with reduction in chronotropic incompetence, but did not affect HRR1min. In conclusion, impaired CR and HRR1min are associated with advanced disease and do not appear to be independent clinical markers indicating high risk status in HC. Improving CR by titrating doses of negative chronotropic agents, myectomy and atrial pacing may be useful to increase exercise capacity in HC patients.
Pericardial disease is a common complication of solid tumors and occasionally seen in hematologic malignancies. Pericardial effusion, when it occurs, is usually caused by tumor seeding of the pericardium leading to a serous effusion or by mass effect from mediastinal lymphadenopathy blocking drainage of lymphatic ducts. Pericardial disease from non-Hodgkin’s lymphoma is uncommon and malignant pericardial effusion is even rarer. Here we present a case of a 31-year-old male with diffuse large B-cell lymphoma who developed cardiac tamponade from a malignant pericardial effusion.
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