HEART FAILURE AND COMORBIDITIES

Comorbidities associated with heart failure include hypertension, myocardial infarction, diabetes, renal failure, metabolic syndrome, and respiratory insufficiencies.

Hypertension

Hypertension is the most common comorbidity of heart failure. Hypertension that includes a chronic BP of >160/90 mmHg increases the life risk of developing HF by 1.6 times that of a usual BP reading of <120/80 mmHg at all ages (Benjamin et al., 2020).

Hypertension reflects increased vascular resistance to the efforts of the heart, especially the left ventricle, to pump blood to the body. The harder the heart works to pump blood, the more work the muscle (myocardium) must do. As with any muscle, the more work required to pump blood, the larger the muscle grows to work effectively. This results in myocardial hypertrophy, creating a larger, less-flexible muscle that must in turn work even harder, causing ventricular remodeling. Ventricular remodeling results in large, oddly shaped contractile cells, increased oxygen consumption, increased cardiac workload, increased wall tension, and impaired contractility (Harding et al., 2020).

Uncontrolled hypertension is also the most common cause of a HF exacerbation. Since it is a modifiable risk factor for heart failure, early recognition and intervention for hypertension helps to prevent further worsening of cardiac function. Managing blood pressure is an essential part of preventative care to avoid the recurrence of aggravated HF symptoms. Blood pressure management is a multifaceted, multidisciplinary approach that includes medications, diet, exercise, and establishment and support of activities of daily living.

Cardiac dilation occurs when a sustained BP elevation causes enlargement in the cardiac chambers, usually the left ventricle. This causes the myocardial fibers to stretch in response to increased volume at the end of diastole. The degree of stretch is related to the force of the contraction during systole (the Frank-Starling law). This is a compensatory mechanism that supports BP, cardiac output, and perfusion, but eventually fails as the patient decompensates and starts to experience HF (Harding et al., 2020).

Myocardial Infarction

Myocardial infarction (MI) is a common comorbidity for heart failure. An MI in the area of the left ventricle (LV) may cause a dysfunctional LV, leading to a drop in cardiac output due to incomplete emptying of the ventricle. This causes the myocardium to have to exert greater effort to pump blood to the rest of the body. After time, this increased effort causes the cardiac pump to be less effective, eventually leading to HF.

Cell injury in the infarcted area causes an inflammatory response. As cardiac output and subsequent renal blood supply drops, the renin-angiotensin-aldosterone system (RAAS) goes into effect. Additionally, the production of antidiuretic hormone (ADH) stimulates further production of the vasoconstrictor endothelin, causing arterial vasoconstriction that will increase cardiac contractility and hypertrophy, intensifying the effects of HF.

Infarcted myocardial tissue becomes akinetic (motionless), causing pump failure (systolic failure, or HFrEF). As discussed earlier in this course, poor coronary artery blood flow causes myocardial ischemia that may lead to an infarction of the myocardial tissue over time. Infarcted tissue is necrotic, losing all former abilities, including contractility. The necrotic tissue is therefore no longer capable of movement, causing a decrease in the strength of the heart to function as a pump. This pump failure affects the amount of blood emptied through force from the affected chamber(s). When the left ventricle is affected, a smaller volume of blood leaving the left ventricle to the aorta affects the ability of the other cardiac chambers to empty, causing congestion.

Diabetes

Diabetes mellitus (DM) is frequently associated with heart failure. The dramatic increase in the number of people diagnosed with diabetes will most likely cause a similar growth in the number of people with HF.

One population study found that those with diabetes had a higher body mass index, plasma insulin level, and serum glucose level than those without diabetes, whereas both sample groups had similar ejection fractions. After a 10.8-year follow-up period, the patients with DM had a 21% incidence of HF compared to a 12% incidence among those without DM (Klajda et al., 2020).

Another correlation between diabetes and HF is that insulin is a powerful sodium-retaining hormone. Patients with type 1 diabetes who are receiving insulin have a greater tendency to retain fluid, thus exacerbating the effects of HF. Patients with type 2 diabetes and HF who are taking empagliflozin (a sodium-glucose transporter 2 inhibitor) showed a reduction in hospitalizations. Those with no HF had a lower incidence of developing the disease over time (Fukuoka et al., 2020).

High blood sugars result in vascular scarring in the layer of the tunica intima affecting circulation. Prolonged periods of uncontrolled blood glucose levels, now recommended to be <150 mg/dL, result in permanent scarring and cause significant impact as blood flow is affected. This may result in poor tissue healing, blindness, renal failure, and HF as the effect of compromised circulation takes its toll on arteries and organ systems over time.

Poor peripheral circulation causes decreased venous return, reducing ventricular filling. Reduced ventricular filling results in a lower cardiac output and reduced ejection fraction. This can cause HF as the cardiac muscle attempts to compensate for the decreased amount of blood volume exiting the left ventricle and the congestion of blood due to sluggish circulation.

Renal Failure

Renal failure is associated with adverse outcomes in patients with HF. Renal dysfunction, defined as an estimated glomerular filtration rate (eGFR) of <60 mL/minute, is highly prevalent in HF patients.

Reduced renal blood flow because of compromised circulation with a reduced ejection fraction may cause the kidneys to perform poorly. A reduced volume of blood passing through the kidneys will reduce the amount of blood to be filtered, resulting in higher levels of waste products, including nitrogenous wastes (i.e., BUN, creatinine).

In HF combined with renal failure, stimulation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) causes the excretion of catecholamines and angiotensin II, among other substances. The release of angiotensin II produces ventricular remodeling. Abnormal neurohormonal responses can also exacerbate the degree of heart failure. The RAAS acts to control blood pressure by promoting fluid retention and vasoconstriction. When cardiac output drops, decreased renal circulation causes the kidneys to release renin, initiating the RAAS response. This causes fluid sodium retention and will increase the blood pressure and the workload in an already failing heart (Harding et al., 2020).

Metabolic Syndrome

Metabolic syndrome is a group of risk factors that may predispose an individual to heart disease, including HF, diabetes, and stroke. It is characterized by a collection of health issues that includes obesity, high triglycerides, high levels of high-density lipoprotein cholesterol, hypertension, and high blood glucose. An individual is considered to have metabolic syndrome if they have at least three of these five factors (Harding et al., 2020; Popa-Fotea et al., 2020).

The progression of HF correlates highly with a patient with metabolic syndrome. Minor increases in serum glucose cause a high risk for HF. Insulin resistance occurs with 60% of patients with HF. Metabolic syndrome correlates with both systolic and diastolic HF (Popa-Fotea et al., 2020).

Respiratory Insufficiency

Many HF patients have respiratory comorbidities such as chronic obstructive pulmonary disease (COPD) or asthma. COPD and asthma are both characterized by respiratory limitations, often caused by inflammation in the airway. Both HF and respiratory patients share several of the same symptoms, such as dyspnea, fatigue, psychological disturbances, deconditioning, and exercise intolerance.

Pleural effusion can be a common complication of HF. Pleural effusion is when the natural fluid between the two layers of the pleura that exists for lubrication becomes excessive secondary to increased pressure in the pulmonary capillaries. The clinical manifestations are dyspnea, cough, and chest pain. These symptoms may imitate symptoms of acute HF and confound a clinician’s ability to diagnose the specific cause of the worsening symptoms unless a physical assessment and diagnostic tests are performed (Harding et al., 2020).