Preventing and Reversing Heart Disease For Dummies. James M. Rippe

The veins ultimately come together in two very large veins, called the inferior vena cava (vee-nuh cay-vuh) and the superior vena cava. The inferior vena cava drains blood from the lower part of the body and superior vena cava drains blood from the upper part of the body. These veins discharge blood into the right atrium of the heart to be pumped into the right ventricle and out to the lungs again to start the whole process over again.

      ✔ The blood: Although blood is not considered part of the cardiovascular system, circulating blood to every cell of the body is the reason the cardiovascular system exists. This red fluid transports oxygen and fuel to the cells and removes waste products. It’s also the delivery vehicle for many specialized cells and biochemicals, including those that contribute to the development of heart disease.

       Keeping the beat: How the nervous system controls heart rate

      

In addition to its internal electrical system, the heart has profound linkages to the nervous system that provide additional control of the heart rate. Two main branches of the involuntary nervous system interact with the heart – the sympathetic nervous system and the parasympathetic nervous system. In simple terms, the sympathetic nervous system helps the heart speed up, and the parasympathetic nervous system helps the heart slow down. They act through direct nerve links to the heart and through the release of chemical substances that reach the heart through the bloodstream.

       Understanding How Heart Disease Begins and Develops

      The human cardiovascular system is wondrously complex. If every element is in balance and working as it should, a state called homeostasis, then the whole system, including the heart and blood vessels, would remain healthy. Unfortunately, multiple factors related to your biology and lifestyle can tip the system out of balance and trigger the development of heart disease. The earliest changes typically start in childhood or adolescence and then silently progress for years before producing changes that can be seen in diagnostic tests or symptoms that you experience. The most common type of cardiovascular disease is atherosclerosis.

       Defining atherosclerosis – the most common form of cardiovascular disease

      Atherosclerosis results from the gradual buildup of fatty deposits called plaque, or lesions, in the interior walls of large and medium-sized arteries. The disease process starts with small changes in the artery wall and takes years to develop to a point where the narrowing arteries may produce symptoms or negatively affect your health.

      Narrowing in the heart’s arteries leads to coronary heart disease (CHD), also called coronary artery disease (CAD). CHD gradually starves the heart muscle of the high level of oxygenated blood that it needs to function properly. A lack of adequate blood supply to the heart typically produces symptoms that range from angina and unstable angina (see “Recognizing angina, or chest pain” and “Defining Unstable Angina” later in this chapter) to heart attack or sudden death. Narrowing of the carotid arteries that carry blood to the brain increases your risk of stroke. Narrowed arteries in your legs or arms results in peripheral artery disease (PAD).

      The term atherosclerosis comes from two Greek words – athero (paste, gruel) and sclerosis (hardness) – that may give you a graphic image of hardened sludge. Not a pretty picture, is it? But it’s an apt image for these deposits of cholesterol, other fats, cellular wastes, platelets, calcium, and other substances. These deposits typically start with fatty streaks and grow to large bumps that distort the artery and block its interior where the blood must flow. Some plaques are stable and others are unstable or vulnerable to cracking or rupturing, which often leads to an artery-blocking blood clot and subsequent heart attack. The sections that follow profile that development process.

      

During the last 15 to 20 years, evidence from extensive population studies and clinical research has increased doctors’ understanding of the many factors and pathways that contribute to the beginnings and progress of atherosclerosis. The next sections provide an overview of medical science’s best understanding right now; however, you need to remember that new studies continually add to the knowledge of this complex, multifaceted disease.

       Triggering the precursors of atherosclerosis

      

Biological factors that contribute to the development of cardiovascular disease are present from birth and perform vital functions that enable the human body to grow and resist infection. As a consequence, all human beings are born with the potential to develop heart disease. The early precursors of atherosclerosis frequently occur in children, teens, and young adults. Fortunately, adopting a heart-healthy lifestyle can usually reverse these early manifestations. The sooner you start, the better, but it’s never too late.

      Current biomedical evidence has led to a consensus that atherosclerosis is a multifactorial chronic inflammatory disease that starts with the dysfunction of and/or injury to the endothelium, which is the inner lining of artery walls. Although only a single-cell-deep layer, the endothelium regulates the normal functioning of the arterial vessel walls. It acts as the traffic cop responding to the many blood-borne influences and biochemical signals that can modify the arterial walls. When any factor stresses or injures the endothelium, it triggers the inflammatory response that activates a variety of immune system signals and cells that rush to repair the damage.

      If this process is triggered just occasionally, then this immune response repairs the damaged cells and shuts down until additional injury occurs. Unfortunately, the damage produced by most risk factors is constant and chronic. Risk factors such as elevated levels of LDL cholesterol and other lipids (fats), high blood pressure, smoking, and insulin resistance and diabetes cause chronic endothelial dysfunction and inflammation, and keep the immune response stuck in the “on” position.

      Inflammation serves as a mediator in the disease progression by recruiting various immune system fighter and repair cells. The exact pathways by which inflammation exerts its influence are emerging from current research. Scientists are looking especially for inflammation markers that may help physicians diagnose and treat people at high risk of CHD in its early stages before symptoms arise, when lifestyle and medical therapies may halt or even reverse the disease.

       Progressing to fatty streaks

      Among the factors causing endothelial dysfunction to progress to atherosclerotic plaque, elevated levels of the certain types of cholesterol, particularly low-density lipoprotein (LDL) cholesterol, and other lipids play a major roll.

      

Here’s an overview of what happens:

      1. Excess LDL cholesterol is deposited on the artery walls.

      As a basic building block for every cell, cholesterol constantly circulates in the blood along with other substances that are vital for life. When blood levels of cholesterol, particularly LDL cholesterol, are too high, excess LDL cholesterol is deposited on the endothelial lining of arteries where special receptor cells latch on to the LDL molecules.

      2. Trapped LDL damages the cells, triggering the body’s immune system into action.

      This trapped LDL can damage the cells by a process called oxidation. The oxidation attracts protective substances related to the immune system. Cells such as macrophages already in artery walls engulf the oxidized excess lipid. (Risk factors also function to create more dangerous LDL particles such as small dense LDL that pass more easily through the endothelial into the first layer of the artery wall, called the intima.)

      3. As the immune system tries to remove excess lipids and repair the damage, yellow fatty streaks appear on the artery walls.

      Soon more circulating fighter cells, known as monocytes, enter the artery lining and transform