Ask Dr. Pat

Congestive Heart Failure in Women

 

2000px-Renin-angiotensin_system_in_man_shadow.svg(Image Source: Wikimedia)

The cornerstone of treatment of heart failure is the use of inhibitors of angiotensin (most commonly angiotensin converting enzyme inhibitors (ACE inhibitors), like Enalapril, which decrease production of angiotensin, improving the complex protein structure of the muscle fiber and lowering the heart’s filling pressures. Diuretics (commonly called “water pills”), like Furosemide, are important for control of CHF symptoms: helping to decrease the congestion in the lungs and extremities by causing increased urination of salt and water. But unlike ACE inhibitors they have no cellular beneficial effects and further may stimulate additional “fight or flight” hormonal response, explaining why traditional heart failure therapy—which depended primarily on diuretics–was associated with such a dismal prognosis.

Once patients begin to feel better with appropriate drug therapy, with near elimination of congestion, beta blockers, like Carveidalol or Metopralol, are introduced. By blocking the effects of the excess adrenaline, these agents also help repair the internal muscle fiber structures. Additionally, they lower the elevated heart rate in CHF. This decrease in heart rate improves the heart’s oxygen uptake and efficiency. When I went to medical school, beta blockers were contraindicated in CHF since adrenaline acutely supports the failing heart. It was not until the early 1990s that courageous investigators in Switzerland taught us the difference between a mild acute worsening of CHF with beta blockers, well tolerated with careful dosing, as opposed to the marked long-term biologic benefit from withdrawal of adrenaline. The original Swiss papers noted normalization of EF in nearly a third of their patients. While not everyone has the same degree of positive response, improvement is generally seen with this treatment plan.

It’s exciting that these newer medical treatments can regenerate and even at times normalize weakened heart muscles. However, a huge caveat is that the medications require a high level of experience to use properly and are often prescribed in inadequate doses. Effective doses are those at, or close to, levels in the original clinical trials. ACE inhibitors and beta blockers are also medications for hypertension, and CHF patients often have low blood pressure to begin with. Coupled with the fact that beta blockers initially can worsen CHF, cardiologists are often reticent about these treatments and prescribe inadequate dosages, relying instead on large diuretic doses. A medical regimen with inadequate doses of ACE inhibitors and beta blockers represents a lost opportunity for improvement in CHF and only produces short-term symptomatic improvement, followed by further deterioration. All too often “advanced therapies” for CHF, like mechanical implants or even transplantation, are contemplated, when an optimal medical regimen would have made such considerations unnecessary. In fact, there are publications from cardiac transplant teams documenting that nearly 40 percent of patients referred for transplant as a last resort improve dramatically with appropriate upward adjustment of their medications and are then removed from the transplant list. The upshot is that optimal treatment of CHF requires an experienced, talented physician and these are most commonly found in a large teaching institution where there is an emphasis on practicing evidence-based and guideline-driven medicine.

In contrast to HF-reduced EF, HF-preserved EF—a condition most commonly seen in older women— has no specific proven therapies. Consequently, the treatment is a bit more art than science. There are, however, some general principles that work. Hypertension and glucose intolerance, while being risk factors for both types of CHF, are directly causal to the hypertrophied stiffened heart in this condition. Aggressive treatment of these factors and correction of the heart rhythm disorders that frequently accompany them, can help control, or possibly completely reverse this condition. While this form of CHF is not quite as lethal, it still has the potential to significantly diminish quality of life. With the aging of the population HF-preserved EF is becoming a more frequent problem, and finally garnering much deserved attention from the medical and pharmaceutical community with hope for better therapies in the future.

While the outlook for patients with CHF has improved dramatically, this chronic problem remains a serious illness whose incidence is rapidly increasing with the aging of the population. The problem has intensified the focus on prevention, which is certainly worth a pound of cure. The current CHF guidelines approach prevention by labeling patients as “Stage A CHF”: those who actually have normal hearts but have risk factors such as hypertension and obesity with glucose intolerance. Embracing lifestyle changes and introducing effective medical management of these abnormalities may potentially have a huge impact on preventing new cases of CHF. Heart artery blockage, or coronary artery disease (see discussion in this publication) is a common cause of CHF and needs to be promptly identified and treated. Unfortunately, as in your case, Pam, the diagnosis of coronary artery disease is frequently delayed in younger women, allowing heart damage to occur, which then sets the stage for the eventual development of CHF. Excessive alcohol intake, certain types of chemotherapy, and even overuse of commonly prescribed anti-inflammatory medications, like Ibuprofen, can damage the heart muscle. Overall, a healthy lifestyle with attention to diet and physical activity, appropriate use of medications for hypertension and glucose intolerance, and early evaluation of potentially cardiac-related symptoms will greatly improve the incidence of CHF, preventing the need for treatment.

 

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