Cardiac fibrosis commonly refers to the excess deposition of extracellular matrix in the cardiac muscle, but the term may also refer to an abnormal thickening of the heart valves due to inappropriate proliferation of cardiac fibroblasts. Fibrotic cardiac muscle is stiffer and less compliant and is seen in the progression to heart failure. The description below focuses on a specific mechanism of valvular pathology but there are other causes of valve pathology and fibrosis of the cardiac muscle. Fibrocyte cells normally secrete collagen, and function to provide structural support for the heart. When over-activated this process causes thickening and fibrosis of the valve, with white tissue building up primarily on the tricuspid valve, but also occurring on the pulmonary valve. The thickening and loss of flexibility eventually may lead to valvular dysfunction and right-sided heart failure. Types
Following are types of myocardial fibrosis:

Interstitial fibrosis, which is unspecific, and has been described in congestive heart failure, hypertension, and normal aging. Subepicardial fibrosis, also unspecific, and is associated with non-infarction diagnoses such as myocarditis and non-ischemic cardiomyopathy. Replacement fibrosis, which indicates an older infarction. Connection with excess blood serotonin (5-HT)
Certain diseases such as neuroendocrine tumor of the small intestine (also known by the obsolete term carcinoid), which sometimes release large amounts of 5-hydroxytryptamine, commonly known as 5-HT or serotonin into the blood, may produce a characteristic pattern of mostly right-sided cardiac fibrosis which can be identified with echocardiography. Cardiac fibrosis is a significant source of morbidity and mortality in patients with functional neuroendocrine tumors.
Combined hyperlipidemia (or -aemia) is a commonly occurring form of hypercholesterolemia (elevated cholesterol levels) characterised by increased LDL and triglyceride concentrations, often accompanied by decreased HDL. : 534  On lipoprotein electrophoresis (a test now rarely performed) it shows as a  hyperlipoproteinemia type IIB. It is the most commonly inherited lipid disorder, occurring in around one in 200 persons. In fact, almost one in five individuals who develop coronary heart disease before the age of 60 have this disorder. The elevated triglyceride levels (>5 mmol/L) are generally due to an increase in very low density lipoprotein (VLDL), a class of lipoproteins prone to cause atherosclerosis. Cause
Hereditary factors are the most common cause. A diet high in saturated fat and cholesterol increases blood cholesterol and triglyceride levels. Other disorders, such as diabetes mellitus, kidney disease, and hypothyroidism, may promote hypertriglyceridemia. Certain drugs, such as estrogen, corticosteroids, retinoids, protease inhibitors, thiazide diuretics, and beta-blockers, may cause hypertriglyceridemia. Obesity increases the risk of hyperlipidemia. Chronic, excessive alcohol use increases the risk of hypertriglyceridemia. Smoking and not exercising may lead to hyperlipidemia. Steroid uses, alcoholism, hypothyroidism, oral contraceptives, chronic kidney failure, hypopituitarism, and nephritic syndrome are other contributors to hyperlipidemia. Diagnosis
Types
The two forms of this lipid disorder are:

Familial combined hyperlipidemia (FCH) is the familial occurrence of this disorder, probably caused by decreased LDL receptor and increased ApoB. Acquired combined hyperlipidemia is extremely common in patients who have other diseases from the metabolic syndrome ("syndrome X", incorporating diabetes mellitus type II, hypertension, central obesity and CH).