Congestive heart failure: pathophysiology and clinical management

Congestive Heart Failure

CHF Overview:

As you know, Congestive Heart Failure (CHF) is one of the most common causes of death in the United States. The multifaceted causes and symptoms associated with CHF often leave the health care provider treating the symptoms rather than underlying causes, with near universal need to tailor care to each patient through a sometimes difficult process if elimination. The sometimes-idiosyncratic nature of epidemiology can also leave the provider with limited options for treatment and care. What is known about the disease is that it is one of the leading chronic conditions associated with mortality and overall healthcare expenditures in the United States, that it strikes most heavily among those over the age of 65 and is more common among black men, white men, black women and white women respectively. (CDC 1994)

Predicting who in the general population or among those with some preexisting cardiac disease will develop CHF has been an elusive goal. However, racial differences in the incidence and progression of CHF and its response to therapy suggest that a genetic component is at play.

Two receptors -- the presynaptic [[alpha].sub.2c]-adrenergic receptor and the postsynaptic [[beta].sub.1]-adrenergic receptor -- work together to control the release of norepinephrine and the resulting force of the heart muscle contraction. Polymorphic variations in these receptors that increase the release of norepinephrine could result in more forceful heart contractions over a period of years, leading to more heart failure. (Phelps 2003)

Additionally the distribution of the disease across the United States varies greatly by state:

In 1990, age-adjusted CHF death rates varied substantially among the states and ranged from 3.7 (Florida) to 31.5 (Alabama) (Table_1). For persons aged greater than or equal to 65 years, state-specific CHF death rates ranged from 29.9 (Florida) to 246.2 (Alabama). (CDC 1994)

One leading expert on CHF states that: "Congestive heart failure is a sequel to various heart diseases and is often the end stage of cardiac disease," (Little 2002) a demonstration of a multifaceted cause and effect disease that often ends with morbidity in its victims. In the same work Little also sites and older study that indicates that: "Half of the patients diagnosed with congestive heart failure will die within 5 years, and one in five persons dies within 1 year." (Little 2002)

In the National Heart, Lung, and Blood Institute. Morbidity & mortality: 2002 chart book on cardiovascular, lung, and blood diseases the estimates of disease occurrence in the United States is 4.8 million people, living with the condition and a new case load of 400,000 persons being diagnosed with CHF every year. (2002) Little, a CDC researcher from the office of Genomics and Disease Prevention, CDC Epidemiology Group, Department of Medicine & Therapeutics, states that:

The incidence does not vary by sex, but it increases with age, with an annual incidence approaching 10 per 1000 after 65 years of age. The prevalence increased substantially during 1976-1991 and is expected to increase because a) as more patients with heart diseases survive with their disease, their opportunity for developing congestive heart failure increases, and b) the elderly population is expected to increase. (Little 2002)

Little goes on to point out the genetic components of the disease, or prevalence among races stating that: "The prevalence is at least 25% greater among the black population than among the white population." (Little 2002) Also according to Little, "During 1971-2000, hospitalization rates attributed to the condition more than tripled for persons aged 45-64 years and 65 years and older." This can in part be due to increased understanding of the disease, its risk factors, genealogical prevalence that in turn have led to earlier detection and ultimately more positive outcomes for patients.

There has been an increased insurgence of research associated with the genetic predisposition of individuals, both animal and human to the development of the disease, bolstered by the hereditary prevalence and the clear racial bias of disease prevalence. In a recent study published in the New England Journal of Medicine Hajjar and MacRae found a substantial link between certain genetic receptors and the development of CHF in lab animals. "Variation in penetrance of familial cardiomyopathy and strain-specific effects in animal models suggest a role for genetic factors in the etiology of congestive heart failure." (Hajjar and MacRae 2002) Another study published in the New England Journal of Medicine also demonstrates the same genetic interactions within a human study of 159 subjects, "variants of the ?2cDel322-325 and ?1Arg389 receptor genes interacted to increase the risk for congestive heart failure." (Small et. al. 2002)

According to the National Heart, Lung, and Blood Institute in the 2002 findings the rates of expense are astronomical and with the obvious growth of the disease the projected findings can be easily assumed to increase with the rates of those living with the chronic disease, "The annual expenditure for health and lost productivity from CHF is estimated to be $23.2 billion." (National Heart, Lung, and Blood Institute 2002) The challenges of treating this disease are many and varied but new technology for both treatment and diagnosis are changing the outcomes for both patients and clinicians.

CHF Treatment:

As you know traditional treatment for CHF has been associated with symptom relief that reduces the load on the cardiac muscle. This includes lifestyle alterations, diet changes, mild exercise and depending on the extreme of the disease chemotherapeutic agents of various types. In most cases non-surgical intervention is the best option, and the treatment options include a list of medications that can be tailored to the specific needs of the patient and his or her symptoms. The goal of all treatment is to reduce the work load on the heart, improve the ability of the heart to pump and to remove the excess fluid within the body, that is both a symptom and a cause for further problems due to heart failure. (Adult Health Advisor 2002)

Medications, which could be prescribed, alone or in combination, are well

Known to the medical community and they include:

ACE inhibitor drugs, to dilate the arteries and allow a more effective blood flow

Beta blockers to reduce the effects of high adrenaline in the body, caused by the heart failure.

Digitalis drugs, which slow the heart rate and allow the heart to pump with a more productive output.

Diuretics which reduce the fluid load on the body.

With all of these chemotherapeutic interventions there are special considerations. ACE inhibitors may become ineffective over time. Beta-blockers might worsen the situation if not titrated with careful consideration and monitoring. Diuretics may reduce the essential elements in the body, such as potassium that can in turn reduce the hearts ability to maintain rhythm and reduce patient's ability to function with any quality of life and Digitalis drugs which can become less effective over time and also reduce the cardiac output to much to quickly by reducing the heart rate to quickly.

Despite possible complications and a complicated set of standards of practice as with nearly all non-surgical interventions the combination of lifestyle change, diet change and medication are still a best possible solution for many people suffering with CHF, especially those who have greater risk for mortality from surgical intervention or who are in the early stages of what will become a chronic disease state. (Adult Health Advisor 2002) The damage that can be done by the progressive decreased production of the heart and all the symptoms caused by it can usually be successfully managed by careful tailored patient care, without surgical intervention and will likely slow the cycle of degeneration caused by the disease process and its damaging symptoms.

Depending on the severity of the case, whether it is acute or chronic and how it is responding to treatment, and the underlying causes most primary care providers and cardiac specialist will recommend a non-surgical intervention. (Adult Health Advisor 2002) Yet, in cases where the CHF is acute and threatening to prematurely end a patients life due to complete organ failure or end stage chronic disease state surgical intervention may be the only alternative.

Surgical intervention includes old standards for heart surgery treatment, including some relatively minor procedures such as angioplasty, with several various surgical additions such as stints, (and even radiation blasts at the site of the stint placement) and valve repair if any valve damage is present. The effectiveness of relatively minor surgical interventions is obvious given the sheer numbers of patients undergoing and achieving successful marked recovery from such surgeries. Yet, the more extreme the case the more extreme the intervention and historically one of the most extreme option is a combination surgery with coronary bypass as the ultimate surgical intervention. Sometimes these interventions also include implantations of pacemakers and defibrillators or technologically advanced combinations of the two, this is commonly known as Arrhythmia Ablation, where the natural electrical impulses of the heart are either bypassed or assisted by implantable devises.

Though in recent years changes have been made in surgical technique. With greater understanding of the disease there have been breakthroughs in treatment both medically and surgically and now the most extreme answer to CHF is a rivalry between four surgical options, all extensive with lengthy lists of contraindications, risks and physical alterations.

Those four surgical options are:

Traditional bypass surgery with or without combination surgical treatments

Implantation of ventricular assist devices

Ventricular Reduction Surgery of two main types

Heart Transplantation

Within these four surgical interventions as is known are many stipulations for action, care and means for recovery.

Traditional bypass surgery as discussed before is an option for many patients with extreme arterial degeneration and possibly valve damage. Yet, the traditional bypass reduces the load on the patients natural heart but does not always reduce the disease process or eliminate the need for further intervention, in the form of additional bypass surgeries or other means of intervention. Though still widely effective and widely practiced, the recovery and extreme nature of the surgical intervention can be deterrents to such an intervention.

The implantation of ventricular assist devices, though not terribly common is become more widely available across the country. As more and more patients undergo bridge to transplant treatment with these devices the research obtained has led to the acceptance of at least one of these devices for permanent implantation. The purpose and function of a ventricular assist device is to bypass the Left Ventricle of the patients natural heart to improve pulmonary cardiac output. The implanted portion of the device is a fist sized titanium pump lined internally with a material that allows the growth of scar tissue that both cushions blood cells and reduces risk of stroke. The contraindications for the implantation of such a device would be a non-functioning right heart and an inability to obtain enough social support to live with and care for a rather complicated device.

The implanted portion of the device is a fist sized titanium pump lined internally with a material that allows the growth of scar tissue that both cushions blood cells and reduces risk of stroke. The power supply of the device is external, the patient is either attached to a large, wall unit that powers the device or they are attached to a double set of lead batteries worn in a sling over the sides and both options are available to the patient at all times. There is also and emergency hand pump, (as well as an injectable emergency anticoagulant used if the power to the device has been removed for longer than two minutes or an unknown amount of time) in the case of complete power failure of both the wall unit and the battery packs. The permanent exit wounds require great care and constant monitoring. Special training is needed and care can seem complicated to both the patient and care providers but the system allows patients to strengthen cardiac output and potentially overall health through bypassing the sick parts of the heart.

The HeartMate VE Left Ventricular Assist Device, described above has recently been approved for non-transplant eligible implantation as well as bridge to transplant patients and other systems are such as the Thoratec LVAD/RVAD/BiVAD, and the Abiomed BVS 5000 LVAD/RVAD/BiVAD are all available in different regions, at different hospitals for bridge to transplant patients. (Strong Health and Vascular Center Web site: (http://www.stronghealth.com/services/surgical/Cardiothoracic/heartfailure.cfm) Most transplant care systems, and a few regional artificial heart teams have vast amounts of information associated with these implantable devices and as the body of research grows so does the technological advances of such devices.

Though traditionally the two greatest possible negative outcomes for patients are stroke, associated with the formation of blood clots inside the assist device, and the failure of an already compromised patient to have functional healing at the pneumatic and electrical exit site wound, a permanent part of the FDA approved HeartMate pneumatic LVAD. The trial studies are well advanced for devices with different working mechanisms and different power supply standards and will undoubtedly become available in the coming years.

Ventricular Mass Reduction Surgery, also known as a Partial Left

Ventriculectomy is a less widely used procedure that has only recently been approved by the FDA for treatment of CHF. The traditional type of Ventricular Mass Reduction Surgery known as the Batista method has a larger scope of surgical intervention than comparative Left Ventricular Aneurysmectomy, where only the dead or ischemic portion of the left ventricle is removed. In early clinical trials comparing the two methods did determine a slightly statistically higher death rate with the Ventricular Reduction Surgery but more work will undoubtedly be done in the future.