RESUMEN
The therapeutical advances in recent years in the field of oncology treatment have increased survival rates and improved the quality of life of oncology patients, thus turning cancer into a chronic disease. However, most of the new cancer treatments come at the expense of serious cardiovascular adverse events threatening the success story of these patients. The establishment of multidisciplinary medical teams to prevent, monitor, and treat cardiovascular diseases in cancer-treated patients is needed now more than ever. The aim of this narrative review is to demonstrate the existing knowledge and practical approaches on how to establish and maintain a cardio-oncology program for the rising number of patients who need it.
RESUMEN
Throughout the last decades, newly developed chemotherapeutic agents and immunotherapies that target signaling pathways have provided patients with better prognoses, improved their quality of life and increased survival rates, thus converting cancer to a stable chronic disease. However, non-anthracycline cancer chemotherapy agents and immunotherapies including human epidermal growth factor receptor 2 (HER2) inhibitors, vascular endothelial growth factor (VEGF) inhibitors, Bcr-Abl tyrosine-kinase inhibitors (TKI), proteasome inhibitors, immune checkpoint inhibitors and chimeric antigen receptor T cells (CAR-T cells) may cause cardiovascular toxicity events and complications that usually interrupt the continuation of an appropriate treatment regimen, which induces life-threatening risks or leads to long-term morbidity. Heart failure, cardiac arrythmias and cardiomyopathies are the most common cardiovascular events related to cardiotoxicity due to chemotherapy. Each patient should be carefully assessed and monitored before, during and after the administration of chemotherapy, to address any predisposing risk factors and the new onset of cardiotoxicity manifestations early and treat them appropriately. The development of novel anticancer agents that cause minimal cardiovascular toxicity events or novel agents that ameliorate the adverse effects of the existing anticancer agents could drastically change the field of cardio-oncology. The aim of this narrative review is to demonstrate new knowledge regarding the screening and diagnosis of non-anthracycline-induced cardiotoxicity and to propose protective measures that could be performed in order to achieve the delivery of optimal care.
RESUMEN
OBJECTIVES: Cardiac magnetic resonance (CMR) imaging is a key test in the diagnosis of cardiac amyloidosis (CA). Extracardiac involvement is common in light chain (AL) amyloidosis and MRI findings may assist in its diagnosis. We sought to investigate the utility of splenic CMR parameters for the diagnosis of CA. METHODS: Thirty-four patients with AL amyloidosis and 32 patients with severe left ventricular hypertrophy in the setting of aortic stenosis (LVH-AS) who completed 3T cardiac MRI at the time of their diagnosis of AL or LVH-AS were assessed with T1, T2 (modified Look-Locker inversion recovery), extracellular volume (ECV) mapping, and late gadolinium enhancement (LGE) imaging of the heart and spleen. RESULTS: Age, left ventricular mass index, wall thickness, ejection fraction, and splenic dimensions did not differ significantly between groups. All AL patients had cardiac involvement. T1 and T2 spleen mapping did not differ significantly between groups but AL patients had higher median ECV in the spleen than in LVH-AS (AL 46.9%, LVH-AS: 31%, p < 0.001), and significantly lower short tau inversion recovery ratio (AL: 1.7, LVH-AS: 2.7, p < 0.001) both with very good diagnostic performance to diagnose AL. We identified 16 AL patients with spleen involvement and 16 without. Spleen ECV and "normalized" spleen ratio, defined as the ratio of spleen LGE to muscle values exhibited strong correlation and had excellent diagnostic performance to discriminate those with spleen involvement. CONCLUSION: Our findings show that spleen CMR parameters can identify spleen involvement in AL patients and differentiate them from those without AL amyloidosis.
RESUMEN
Myocardial involvement has been described during previous SARS and MERS outbreaks. Infection by SARS-CoV-2 (COVID-19) can range from asymptomatic to life-threatening multi-system disease. Heart involvement most commonly occurs during severe COVID-19 infection. Myocardial injury, based on elevated levels of myocardial enzymes, has been noted in up to 30% of patients with COVID-19 infection and could be a marker for worse prognosis. A few cases of possible myocarditis due to SARS-CoV-2 have been described, providing variable degree of evidence of direct myocardial involvement. We reviewed in detail those cases in comparison to relevant literature on SARS and MERS and attempted to draw initial conclusions in regard to clinical presentation, treatment and prognosis.
RESUMEN
The unfolding COVID-19 pandemic began in December 2019 in Wuhan, Hubei Province. COVID-19 is a systemic infection affecting several systems including the haematopoietic system. Surveys illustrating the laboratory findings of these patients conclude that lymphocytopenia, neutrophilia and thrombocytopenia are prominent amongst them. Moreover, it has been reported a significant decrease in T lymphocyte subsets and an increase of inflammatory cytokines of hospitalized patients with COVID-19. Generally, thrombocytopenia is commonplace in critically ill patients and usually suggests serious organ malfunction. In view of this, this review investigates the correlation between these abnormalities and the prognosis and disease course. Full blood count is an easy, economic and widely available tool which may help to discriminate between patients with or without severe disease. Last but not least, this review examines potential pathophysiological mechanisms by the novel coronavirus which contribute to these haematological alterations aiding the clinicians to better understand this disease and provide more clinical treatment options.
