Non-invasive cardiac imaging for evaluation of cardiotoxicity in cancer patients - early detection and follow-up

Cardiotoxicity is an increasingly important clinical entity that occurs as a result of untoward, and incompletely understood, effects on cardiac function. It is primarily caused by the anthracycline agents (doxorubicin, daunorubicin) but has also been observed with monoclonal antibody agents such as trastuzumab and small molecule tyrosine kinase inhibitors. The most feared net result of these agents is left ventricular (LV) dysfunction resulting in symptomatic congestive heart failure (CHF). Other manifestations can include arrhythmias, pericardial constriction, valvulopathy and hypertension. Standard cardiac imaging techniques have largely focused on LV ejection fraction (LVEF) quantifi cation. Contemporary cardiac imaging technologies now exist that are capable of evaluating for and detecting earlier stages of cardiotoxicity, including those which occur prior to changes in LVEF. Therapeutic algorithms have been devised to tailor chemotherapeutic regimens based on these results and have resulted in a dramatically reduced incidence of overt CHF

Cancer drugs: Highlighting the molecular mechanisms of cardiotoxicity

The treatment options for patients with cancer have increased rapidly in the last decade with the introduction of newer chemotherapy drugs, targeted agents and monoclonal antibodies. Most of these drugs are aimed at interrupting proliferative signalling, with consequent apoptosis of cancer cells. Because most of the new drugs are multi-targeted, there is a likelihood of so called “off target” effects, where other kinases which are not the primary targets of the drug, are also inhibited. This has led to unforeseen toxicities and, in this commentary, we will focus on the molecular mechanisms underlying cardiotoxicities as a result of cancer therapies. However, cardiotoxicity is not a new concern as the older generation chemotherapies, like anthracyclines, are known to commonly cause irreversible cardiomyopathy, mostly as a result of induced DNA damage and oxidative stress. Over the years, clinicians have adopted some methods of diminishing the incidence of this side-effect and therefore improving patient safety. Trying to decipher the complicated pathways underlying cardiotoxicity helps the scientifi c community to design new drugs that are tumoricidal, whilst sparing normal tissue and as such limiting unwanted side-effects. This has become ever so important, as oncologists cure more patients of cancer, and some previously incurable cancers are increasingly being converted into chronic illnesses. A relationship between the cardiologist and the oncologist has become mandatory to ensure close monitoring of such patients and offering appropriate management, should cardiotoxicities arise

Stress-induced cardiomyopathy complicating severe babesiosis

A post-menopausal lady with severe babesiosis developed a basal-type stress-induced cardiomyopathy. Left ventricular function normalized at three months. We believe this is the first reported case of stress cardiomyopathy complicating severe babesiosis. Cardiac biomarker elevation disproportionate to the area of myocardial dysfunction, electrocardiographic changes, the patient’s clinical condition, and close follow-up of left ventricular function parameters are all vital in diagnosing stress cardiomyopathy and may exclude the need for coronary angiography. There may be a possible association between severe babesiosis and stress cardiomyopathy. (Cardiol J 2011; 18, 1: 83-86

The common apolipoprotein A-1 polymorphism −75A>G is associated with ethnic differences in recurrent coronary events after recovery from an acute myocardial infarction

Since data regarding the relationship between a common polymorphism (SNP) of the apoA1 gene with apoA1 levels and risk of coronary artery disease are inconsistent, we hypothesized that its association with recurrent coronary events differs for White and Black individuals with diagnosed coronary heart disease. The apoA1 −75G>A SNP was genotyped in a cohort of 834 Black (n=129) and White (n=705) post-myocardial infarction patients. Recurrent coronary events (coronary-related death, non-fatal myocardial infarction, or unstable angina) were documented during an average follow-up of 28 months. Thirty percent of White and 21% of Black patients carried the SNP. Cox proportional-hazards regression analysis, adjusting for clinical and laboratory covariates, demonstrated that the SNP was not associated with recurrent events in the total cohort (HR=1.37, 95% CI 0.95–1.97; p= 0.09) but was the only variable associated with an increased risk of recurrent cardiac events in Blacks (HR=2.40, 95% CI 1.07–5.40; p= 0.034). Conversely in Whites, the SNP was not associated with recurrent events (HR=1.12, 95% CI 0.75–1.67; p= 0.59) whereas apoB (HR=1.78, 95% CI 1.20 −2.65; p= 0.0042) and calcium channel blocker use (HR=2.53, 95% CI 1.72–3.72; p<0.001) were associated; p= 0.0024 for interaction between ethnicity and the SNP. A common apoA1 SNP is associated with a significantly increased risk of recurrent cardiac events among Black, but not White, postmyocardial infarction patients. Relationships with lipoproteins may help explain this finding