Cirrhotic cardiomyopathy (CCM) is defined as systolic or diastolic dysfunction in the absence of prior heart disease or another identifiable cause in patients with cirrhosis, in whom it is an important determinant of outcome. Its underlying pathogenic/pathophysiological mechanisms are rooted in two distinct pathways: 1) factors associated with portal hypertension, hyperdynamic circulation, gut bacterial/endotoxin translocation and the resultant inflammatory phenotype; 2) hepatocellular insufficiency with altered synthesis or metabolism of substances such as proteins, lipids, carbohydrates, bile acids and hormones. Different criteria have been proposed to diagnose CCM; the first in 2005 by the World Congress of Gastroenterology, and more recently in 2019 by the Cirrhotic Cardiomyopathy Consortium. These criteria mainly utilised echocardiographic evaluation, with the latter refining the evaluation of diastolic function and integrating global longitudinal strain into the evaluation of systolic function, an important addition since the haemodynamic changes that occur in advanced cirrhosis may lead to overestimation of systolic function by left ventricular ejection fraction. Advances in cardiac imaging, such as cardiac magnetic resonance imaging and the incorporation of an exercise challenge, may help further refine the diagnosis of CCM. Over recent years, CCM has been shown to contribute to increased mortality and morbidity after major interventions, such as liver transplantation and transjugular intrahepatic portosystemic shunt insertion, and to play a pathophysiologic role in the genesis of hepatorenal syndrome. In this review, we discuss the pathogenesis/pathophysiology of CCM, its clinical implications, and the role of cardiac imaging modalities including MRI. We also compare diagnostic criteria and review the potential diagnostic role of electrocardiographic QT prolongation. At present, no definitive medical therapy exists, but some promising potential treatment strategies for CCM are reviewed.

The diagnosis and management of cardiovascular complications have become a clinical concern for oncologists, cardiologists, surgeons, interventional radiologists, radiation therapy physicians, internists, nurses, pharmacists, administrators, and all the stakeholders involved in the care of cancer patients. Anticancer therapies have extended the lives of patients with cancer, but for some this benefit is attenuated by adverse cardiovascular effects. This review article aims to provide an overview of the rationale of setting up a cardio-oncology unit and reflect on our own experience establishing this service, and conclude with some fundamental aspects of consideration for evaluation and management of patients with cancer and cardiovascular diseases. Cardiotoxicity can lead to congestive heart failure and cardiac death. In fact, chemotherapy-related cardiac dysfunction may carry one of the worst prognoses of all types of cardiomyopathies, and has a profound impact on morbidity and mortality in oncology patients. Other complex clinical situations involve cancer patients who might benefit from a highly curative drug in terms of cancer survival but face limitations of its administration because of concomitant cardiovascular diseases. Indeed, the balance between the benefits and risks of the cancer therapy regimen in the context of the cardiovascular status of the individual patient can sometimes be extraordinarily challenging. A subspecialty with a multidisciplinary integrative approach between oncologists, hematologists, cardiologists, among others has thus emerged to address these issues, termed cardio-oncology. Cardio-oncology addresses the spectrum of prevention, detection, monitoring and treatment of cancer patients with cardiovascular diseases, or at risk for cardiotoxicity, in a multidisciplinary manner. In this field, cardiologists assist oncologists and hematologists with cardiovascular recommendations. This can be mediated through e-consultations or face-to-face evaluations. Cardio-oncology is a subspecialty that assists in the overall care of cancer patients with and without cardiovascular disease in an interdisciplinary fashion. We believe that this partnership of sharing responsibilities and experiences among health-care team members can potentially decrease cancer therapeutics-related cardiovascular complications and improve clinical outcomes.

Detection of atrial fibrillation after ischemic stroke is challenging due to its paroxysmal nature. We aimed to assess predictors of paroxysmal atrial fibrillation using non-invasive surface ECG and transthoracic echocardiography to select candidates for atrial fibrillation screening. Ischemic stroke patients without documented atrial fibrillation (n = 110, 67 ± 10 years, 40 female) and a control group of age- and gender-matched patients with history of paroxysmal atrial fibrillation prior to stroke (n = 55, 67 ± 10 years, 19 female) comprised the study sample. Using non-invasive ECG monitoring for three weeks, short episodes of paroxysmal atrial fibrillation were detected in 24 of 110 patients (22 %). The standard 12-lead ECG with sinus rhythm at stroke onset was digitally processed and analyzed. Transthoracic echocardiography data were reviewed for these patients. Atrial fibrillation history was independently associated with P terminal force in lead V 1 > 40 mm*ms (OR 4.04 95 % CI 1.34–12.14, p = 0.013) and left atrial volume index (OR 1.08 95 % CI 1.03–1.13, p = 0.002; for LAVI > 40 mL/m2 OR 6.40 95 % CL 1.47–27.91, p = 0.013). Among patients without atrial fibrillation history, no ECG characteristics were predictive of atrial fibrillation detected after stroke. Left atrial volume index remained an independent predictor of atrial fibrillation detected after stroke (OR 1.09 95 % CI 1.02–1.16, p = 0.017). A cutoff of <40 mL/m2 had an 84 % negative predictive value for ruling out atrial fibrillation on ambulatory monitoring with a sensitivity of 50 % and a specificity of 86 %. In a post hoc analysis, left atrial dilatation assessed by left atrial volume index independently predicted atrial fibrillation after stroke in patients without prior atrial fibrillation history, while the other clinical or ECG markers were not predictive of atrial fibrillation detected early after ischemic stroke. This study is a post hoc analysis from the prospective case-control study registered in December 2011, ClinicalTrials.gov ID: NCT01325545 .

Objective Graves’ disease (GD) can both aggravate pre-existing cardiac disease and cause de novo heart failure (HF), but large-scale studies are lacking. We aimed to investigate the incidence, risk factors and outcomes of incident GD-related HF. Methods Patients with GD (2009–2019) were retrospectively included. HF with reduced ejection fraction (HFrEF) was defined by left ventricular ejection fraction <50% and Framingham criteria, while HF with preserved ejection fraction (HFpEF) was defined according to the HFA-PEFF criteria. HF due to ischaemia, valve disorder or other structural heart disease was excluded. Proportional hazards regression was used to analyse risk factors and outcomes. Results Of 1371 patients with GD, HF occurred in 74 (5.4%) patients (31 (2.3%) HFrEF; 43 (3.1%) HFpEF). In HFrEF, atrial fibrillation (AF) (HR 10.5 (3.0–37.3), p<0.001) and thyrotropin receptor antibody (TRAb) level (HR 1.05 (1.01–1.09) per unit, p=0.007) were independent risk factors. In HFpEF, the independent risk factors were chronic obstructive pulmonary disease (HR 7.2 (3.5–14.6), p<0.001), older age (HR 1.5 (1.2–2.0) per 10 years, p=0.001), overt hyperthyroidism (HR 6.4 (1.5–27.1), p=0.01), higher body mass index (BMI) (HR 1.07 (1.03–1.10) per unit, p=0.001) and hypertension (HR 3.1 (1.3–7.2), p=0.008). The risk of cardiovascular hospitalisations was higher in both HFrEF (HR 10.3 (5.5–19.4), p<0.001) and HFpEF (HR 6.7 (3.7–12.2), p<0.001). However, only HFrEF was associated with an increased risk of all-cause mortality (HR 5.17 (1.3–19.9), p=0.02) and ventricular tachycardia/fibrillation (HR 64.3 (15.9–259.7), p<0.001). Conclusion De novo HF occurs in 5.4% of patients with GD and is associated with increased risk of cardiovascular hospitalisations and mortality. Risk factors include AF, higher TRAb, higher BMI and overt hyperthyroidism.