Learn how you can manage and alleviate your current side effects while actively working to prevent a relapse or secondary cancer using evidence-based, non-toxic therapies.
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Chemotherapy-induced cardiomyopathy. Congestive Heart Failure. In short, lots of aggressive cardio toxic chemotherapy regimens weakened my heart. So much so that I also developed atrial fibrillation.
If you are a cancer survivor who underwent cardio toxic chemotherapy as well, you have a growing risk of cardiomyopathy and congestive heart failure. But…there’s hope.
I’ve managed my heart failure since late 2010 with no conventional medications. I didn’t react well to metoprolol. I had such as bad experience with the short, long-term and late stage side effects caused by my many chemo regimens that I decided to undergo evidence-based but non-toxic heart therapies. And all my heart metrics have improved over the years (ejection fraction, BP, even my aortic root and AA- all have improved).
I do not want to paint a rosey picture of my CHF. I exercise moderately but daily. I eat a heart healthy diet. I drink only a little wine each week. I take many different supplements daily shown to benefit my heart function.
I frequently blog about my approach to managing my heart in hopes that other cancer survivors with chemotherapy-induced cardiomyopathy and a growing risk of Congestive Heart Failure will want to improve their own heart health- with or without conventional heart meds.
Are you a cancer survivor? Did you undergo one of many different cardio toxic chemotherapy regimens? Are you worried about your long-term heart health and the possibility of congestive heart failure? Scroll down the page, post a question or comment and I will reply to you ASAP.
“Despite the majority of children in the US surviving cancer, some children can be left with diseases typically observed in older adults and why this occurs is not fully understood. Why is this?
On average, age-related chronic health conditions occur much earlier among survivors than in the non-cancer general population. For example, a survivor at age of 35 years may be comparable to a non-cancer individual at age of 50 years regarding the risk of developing cardiovascular disease. However, not all survivors showed the same level of aging acceleration and hence the risk.
We use an aging biomarker (e.g., epigenetic age) to objectively measure the biological age of each survivor and try to show that biological aging may account for the difference from one survivor to the other in terms of developing age-related chronic diseases.
You have previously evaluated non-genetic risk factors for this accelerated aging. What did you discover from this previous research and why did your team choose to focus on the underlying genetic factors this time?
Our previous research showed that prior cancer treatment exposures and health behaviors would affect accelerated aging. These are non-genetic factors and can be used in identifying survivors with higher accelerated aging. For example, a survivor previously treated with irradiation to the chest or adopted an unhealthy lifestyle.
From the literature, we know that biological aging is also partially determined by inherited genetics. So, we conducted this research to search for genetic factors. In the future, we will be able to utilize both genetic factors and non-genetic factors to improve the precision in the identification of survivors with higher accelerated aging.
In your latest research, you investigated accelerated aging in pediatric cancer survivors. Can you describe how you carried out your latest research and what you discovered?
We took advantage of the preexisting whole-genome sequencing data and employed a genome-wide association study (GWAS) approach to agnostically search genetic variations that are strongly correlated with epigenetic age acceleration.
We identified two statistically significant genetic markers, with one mapped to the SELP gene which encodes P-selectin, and the other mapped to the HLA region which encodes genes that are important for immune functions.
In your research, you used data from childhood cancer survivors enrolled in the St. Jude Lifetime Cohort Study (SJLIFE). How important are datasets like this in furthering our understanding of disease and illness?
It is critically important to have a resource like the St. Jude Lifetime Cohort Study to allow investigators to perform survivorship research so we can understand the long-term effects of treatment toxicity, accelerated aging trajectories, as well as the pathophysiology of the chronic disease development.
What effects does this accelerated chronological age have on these pediatric cancer survivors?
Accelerated aging will lead to early-onset of age-related chronic health conditions and premature mortality among pediatric cancer survivors.
” Unfortunately, these agents also exhibit a well-recognized cumulative-dose related cardiotoxic profile that limits the extent to which they can be used safely. In clinical practice, most clinicians limit the cumulative dose of doxorubicin (the most widely used agent in this group) to 400–450 mg/m2, but considerable cardiac damage is now known to occur at cumulative dosages considerably below this level…
Antracycline-induced cardiotoxicity was first described in the 1970s. At that time anthracycline-associated cardiotoxicity was thought of as a cumulative dose-related form of congestive heart failure (CHF) that was rapidly progressive if use of the agent was continued. Von Hoff et al (1979) provided important initial insight regarding clinically manifested CHF. Increased awareness of sub-clinical cardiac impairment resulting from these agents has led to improved screening as well as a better perspective of the inherent toxicity of these agents. Today’s definition has expanded from the clinical events of cardiac failure to include a wide spectrum of predefined laboratory values even when patients may be asymptomatic. These include histological changes (Billingham and Bristow 1984) in the cardiomyocytes (Table 2), and changes in left ventricular ejection fraction (LVEF) based on either radionuclide ventriculography (Schwartz et al 1987) (RNVG) or two-dimensional (2D)-echocardiography (Stoddard et al 1992). Even transient changes previously thought to be not of any major clinical significance, eg, daunorubicin-induced myocarditis/pericarditis (Topalov et al 1981; Gaudin et al 1993) will now be considered as anthracycline-induced cardiomyopathy. The general consensus is that a decrease in LVEF by more than 20 percentage points to a value >50%, a decrease in LVEF by more than 10 percentage points to a value <50%, or clinical manifestations with signs and symptoms of Congestive Heart Failure constitute cardiotoxicity. Others have combined these criteria to define cardiotoxicity as a decrease in LVEF by more than 10 points to a final value of <50% (Ganz et al 1993)…
Using the refined criteria, in large clinical trials, approximately
The incidence of clinical cardiac failure increases precipitously above 550 mg/m2 (Von Hoff et al 1979) with the majority developing cardiomyopathy within the first year of completion of treatment.
More recent data, however, suggest that cardiomyopathy (Congestive Heart Failure) not only develops at a much lower cumulative dose than previously thought, but it may also manifest even years after treatment, especially in pediatric oncology survivors (Lipshultz et al 1991; Steinherz et al 1991; Hequet et al 2004).
An analysis by Steinherz et al (1991) of 201 long-term childhood cancer survivors 4–20 years after completion of anthracycline-based chemotherapy showed almost a quarter of the patients remain at risk for developing cardiomyopathy even years after exposure. Cardiac biopsy as well as newer imaging techniques suggest that cardiac damage almost certainly takes place from the onset of anthracycline exposure irrespective of its detection by conventional non-invasive cardiac parameters…