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.

Cardio-oncology is a medical discipline that identifies, prevents, and treats the cardiovascular complications related to cancer therapy. Due to the remarkable proliferation of new cancer therapies causing cardiovascular complications, such as hypertension, heart failure, vascular complications, and cardiac arrhythmia, we provide an extensive, comprehensive revision of the most up-to-date scientific information available on the cardiovascular complications associated with the use of newer, novel chemotherapeutic agents, including their reported incidence, suggested pathophysiology, clinical manifestations, potential treatment, and prevention. The authors consider this topic to be relevant for the clinicians since cardiovascular complications associated with the administration of recently approved drugs are relatively underappreciated.The purpose of this article is to provide a state-of-the-art review of cardiovascular complications associated with the use of newer, novel chemotherapeutic agents and targeted therapies, including their reported incidence, suggested pathophysiology, clinical manifestations, potential treatment, and prevention. Ongoing efforts are needed to provide a better understanding of the frequency, mechanisms of disease, prevention, and treatment of cardiovascular complications induced by the newer, novel chemotherapeutic agents. Development of a cardio-oncology discipline is warranted in order to promote task forces aimed at the creation of oncology patient-centered guidelines for the detection, prevention, and treatment of potential cardiovascular side effects associated with newer cancer therapies.

Takotsubo syndrome (TTS) is characterized by transient, regional systolic dysfunction of the left ventricle, often mimicking acute coronary syndrome. Atypical variants of this syndrome with mid-ventricular, basal, and focal wall motion patterns are increasingly diagnosed and show different clinical features compared to typical TTS. Even though TTS was generally considered a benign condition, continuous and strict monitoring is necessary to diagnose potentially life-threating complications. This is the first case report, to our knowledge, of atypical TTS in a patient with Goodpasture syndrome triggered by acute kidney injury (AKI).

Endothelial biomarkers are gaining interest in the stratification of cardiovascular risk and early diagnosis of cardiotoxicity secondary to antineoplastic drugs. Interestingly, some drugs, such as anthracyclines, have been recently associated with vascular damage, which reveals the pivotal role of research in identifying biomarkers that could potentially be included into more specific cardiotoxicity risk scores. An extensive report of the incidences of cardiovascular adverse effects of oncologic drugs is presented, with the main purpose of highlighting not only the risk of developing heart failure but also the importance of associated vascular adverse effects (i.e., hypertension, venous, and arterial thrombosis) experienced by patients in the post-chemotherapy phase.

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Introduction: Hypertrophic Cardiomyopathy (HCM) is known as one of the most common causes of sudden cardiac death. Its propensity to lethal arrhythmias is a result of myocardial remodeling leading to aberrant conduction and increased reentrant electrical activity. Previous studies suggest an association between the amount of myocardial fibrosis found on Cardiac Magnetic Resonance (CMR) and the risk of these ventricular arrhythmias. Signal Average Electrocardiography ( SAECG) is a noninvasive technique used to detect subtle conduction abnormalities that can be missed on standard Electrocardiography ( ECG ). Hypothesis: Non-uniform conduction through fibrotic tissue seen in CMR leads to unsynchronized myocardial depolarization which correlates with further repolarization abnormalities that can be detected by SAECG. Method: In this retrospective study, results of SAECG were used to classify 73 HCM patients into Normal or Abnormal groups based on the presence of two or more of three predetermined criteria (fQRS, RMS40, LAS40). Replacement fibrosis was assessed by measuring late gadolinium enhancement (LGE) . Interstitial fibrosis was assessed by measuring T1 relaxation times, using the Look-Locker sequence. Results: A statistically significant association between the presence of myocardial fibrosis on CMR and abnormal SAECG was found with a difference of proportions of 41.3% between the subgroups. Left ventricular mass index was found to be significantly higher in the abnormal subgroup (Normal: 61.2 ± 19.6; Abnormal: 82.4 ± 37.1; p = <0.003, CI 95% [2.93; 39.47]). The presence of T wave inversions on standard ECG was only seen in those who had an abnormal SAECG exam. Conclusion: Abnormal SAECG in patients with HCM is associated with the presence of LGE on CMR. This study showed a subset of patients with absence of LGE despite having abnormal SAECG, which implies that there are other complex mechanisms besides replacement fibrosis, that predisposes this population to ventricular arrhythmias. This can also be highlighted by the fact that there was no difference between the two groups in the T1 mapping time. We believe that SAECG could be an objective assessment of the arrhythmogenic substrate present in patients with HCM.