Particulate matter has been studied for its short- and long-term exposure effects on cardiovascular disease. Currently, PM is the major focus, in which gradients are used to determine CVD risk. For every 10 μg/m of PM long-term exposure, there was an estimated 8–18% CVD mortality risk. Women had a higher relative risk (RR) (1.42) for PM induced coronary artery disease than men (0.90) did. Overall, long-term PM exposure increased rate of atherosclerosis and inflammation. In regards to short-term exposure (2 hours), every 25 μg/m of PM resulted in a 48% increase of CVD mortality risk. In addition, after only 5 days of exposure, a rise in systolic (2.8 mmHg) and diastolic (2.7 mmHg) blood pressure occurred for every 10.5 μg/m of PM. Other research has implicated PM in irregular heart rhythm, reduced heart rate variability (decreased vagal tone), and most notably heart failure. PM is also linked to carotid artery thickening and increased risk of acute myocardial infarction.

The cause of cardiomegaly is not well understood and many cases of cardiomegaly are idiopathic (having no known cause). Prevention of cardiomegaly starts with detection. If a person has a family history of cardiomegaly, one should let one's doctor know so that treatments can be implemented to help prevent worsening of the condition. In addition, prevention includes avoiding certain lifestyle risk factors such as tobacco use and controlling one's high cholesterol, high blood pressure, and diabetes. Non-lifestyle risk factors include family history of cardiomegaly, coronary artery disease (CAD), congenital heart failure, Atherosclerotic disease, valvular heart disease, exposure to cardiac toxins, sleep disordered breathing (such as sleep apnea), sustained cardiac arrhythmias, abnormal electrocardiograms, and cardiomegaly on chest X-ray. Lifestyle factors which can help prevent cardiomegaly include eating a healthy diet, controlling blood pressure, exercise, medications, and not abusing alcohol and cocaine. Current research and the evidence of previous cases link the following (below) as possible causes of cardiomegaly.

The most common causes of Cardiomegaly are congenital (patients are born with the condition based on a genetic inheritance), high blood pressure which can enlarge the left ventricle causing the heart muscle to weaken over time, and coronary artery disease that creates blockages in the heart's blood supply, which can bring on a cardiac infarction (heart attack) leading to tissue death which causes other areas of the heart to work harder, increasing the heart size.

Other possible causes include:

- Heart Valve Disease

- Cardiomyopathy (disease to the heart muscle)

- Pulmonary Hypertension

- Pericardial Effusion (fluid around the heart)

- Thyroid Disorders

- Hemochromatosis (excessive iron in the blood)

- Other rare diseases like Amyloidosis

- Viral infection of the heart

- Pregnancy, with enlarged heart developing around the time of delivery (peripartum cardiomyopathy)

- Kidney disease requiring dialysis

- Alcohol or cocaine abuse

- HIV infection

- Diabetes

Cardiovascular disease affects low- and middle-income countries even more than high-income countries. There is relatively little information regarding social patterns of cardiovascular disease within low- and middle-income countries, but within high-income countries low income and low educational status are consistently associated with greater risk of cardiovascular disease. Policies that have resulted in increased socio-economic inequalities have been associated with greater subsequent socio-economic differences in cardiovascular disease implying a cause and effect relationship. Psychosocial factors, environmental exposures, health behaviours, and health-care access and quality contribute to socio-economic differentials in cardiovascular disease.

Known environmental factors include certain infections during pregnancy such as Rubella, drugs (alcohol, hydantoin, lithium and thalidomide) and maternal illness (diabetes mellitus, phenylketonuria, and systemic lupus erythematosus).

Being overweight or obese increases the risk of congenital heart disease. Additionally, as maternal obesity increases, the risk of heart defects also increases. A distinct physiological mechanism has not been identified to explain the link between maternal obesity and CHD, but both prepregnancy folate deficiency and diabetes have been implicated in some studies.

The cause of congenital heart disease may be genetic, environmental, or a combination of both.

The following table includes the main types of valvular stenosis and regurgitation. Major types of valvular heart disease not included in the table include mitral valve prolapse, rheumatic heart disease and endocarditis.

Tetralogy of Fallot occurs approximately 400 times per million live births and accounts for 7 to 10% of all congenital heart abnormalities.

Due to non-compaction cardiomyopathy being a relatively new disease, its impact on human life expectancy is not very well understood. In a 2005 study that documented the long-term follow-up of 34 patients with NCC, 35% had died at the age of 42 +/- 40 months, with a further 12% having to undergo a heart transplant due to heart failure. However, this study was based upon symptomatic patients referred to a tertiary-care center, and so were suffering from more severe forms of NCC than might be found typically in the population. Sedaghat-Hamedani et al. also showed the clinical course of symptomatic LVNC can be severe. In this study cardiovascular events were significantly more frequent in LVNC patients compared with an age-matched group of patients with non-ischaemic dilated cardiomyopathy (DCM). As NCC is a genetic disease, immediate family members are being tested as a precaution, which is turning up more supposedly healthy people with NCC who are asymptomatic. The long-term prognosis for these people is currently unknown.

Untreated, tetralogy of Fallot rapidly results in progressive right ventricular hypertrophy due to the increased resistance caused by narrowing of the pulmonary trunk. This progresses to heart failure which begins in the right ventricle and often leads to left heart failure and dilated cardiomyopathy. Mortality rate depends on the severity of the tetralogy of Fallot. If left untreated, TOF carries a 35% mortality rate in the first year of life, and a 50% mortality rate in the first three years of life. Untreated TOF also causes delayed growth and development, including delayed puberty.

Patients who have undergone total surgical repair of tetralogy of Fallot have improved hemodynamics and often have good to excellent cardiac function after the operation with some to no exercise intolerance (New York Heart Association Class I-II). Surgical success and long-term outcome greatly depend on the particular anatomy of the patient and the surgeon's skill and experience with this type of repair.

Ninety percent of people with total repair as babies develop a progressively leaky pulmonary valve later in life. It is recommended that they follow up at a specialized adult congenital heart disease center.

In terms of the cause of pulmonary atresia, there is uncertainty as to what instigates this congenital heart defect. Potential risk factors that can cause this congenital heart defect are those the pregnant mother may come in contact with, such as:

- Certain medications

- Diet

- Smoking

Inflammation of the heart valves due to any cause is called valvular endocarditis; this is usually due to bacterial infection but may also be due to cancer (marantic endocarditis), certain autoimmune conditions (Libman-Sacks endocarditis, seen in systemic lupus erythematosus) and hypereosinophilic syndrome (Loeffler endocarditis). Certain medications have been associated with valvular heart disease, most prominently ergotamine derivatives pergolide and cabergoline.

Valvular heart disease resulting from rheumatic fever is referred to as "rheumatic heart disease". Damage to the heart valves follows infection with beta-hemolytic bacteria, such as typically of the respiratory tract. Pathogenesis is dependent on cross reaction of M proteins produced by bacteria with the myocardium. This results in generalized inflammation in the heart, this manifests in the mitral valve as vegetations, and thickening or fusion of the leaflets, leading to a severely compromised buttonhole valve.

Rheumatic heart disease typically only involves the mitral valve (70% of cases), though in some cases the aortic and mitral valves are both involved (25%). Involvement of other heart valves without damage to the mitral are exceedingly rare.

While developed countries once had a significant burden of rheumatic fever and rheumatic heart disease, medical advances and improved social conditions have dramatically reduced their incidence. Many developing countries, as well as indigenous populations within developed countries, still carry a significant burden of rheumatic fever and rheumatic heart disease and there has been a resurgence in efforts to eradicate the diseases in these populations.

If untreated, severe symptomatic aortic stenosis carries a poor prognosis with a 2-year mortality rate of 50-60% and a 3-year survival rate of less than 30%. Prognosis after aortic valve replacement for people who are younger than 65 is about five years less than that of the general population; for people older than 65 it is about the same.

In Heyde's syndrome, aortic stenosis is associated with gastrointestinal bleeding due to angiodysplasia of the colon. Recent research has shown that the stenosis causes a form of von Willebrand disease by breaking down its associated coagulation factor (factor VIII-associated antigen, also called von Willebrand factor), due to increased turbulence around the stenotic valve.

A PDA is sometimes idiopathic. Known risk factors include:

- Preterm birth

- Congenital rubella syndrome

- Chromosomal abnormalities (e.g., Down syndrome)

- Genetic conditions such as Loeys-Dietz syndrome (would also present with other heart defects), Wiedemann-Steiner syndrome, and CHAR syndrome.

The epidemiology of pulmonary valve stenosis can be summed up by the congenital aspect which is the majority of cases, in broad terms PVS is rare in the general population.

Bicuspid aortic valves are the most common cardiac valvular anomaly, occurring in 1–2% of the general population. It is twice as common in males as in females.

Bicuspid aortic valve is a heritable condition, with a demonstrated association with mutations in the NOTCH1 gene. Its heritability (formula_1) is as high as 89%. Both familial clustering and isolated valve defects have been documented. The incidence of bicuspid aortic valve can be as high as 10% in families affected with the valve problem..Recent studies suggest that BAV is an autosomal dominant condition with incomplete penetrance. Other congenital heart defects are associated with bicuspid aortic valve at various frequencies, including coarctation of the aorta.

Aortic stenosis in the Rottweiler appears to be true subvalvular aortic stenosis (SAS), similar to that in the Newfoundland dog, as opposed to the valvular form (seen more in boxer dogs) or the supravalvular form sometimes seen in people.

DORV affects between 1% and 3% of people born with congenital heart defects.

Chromosomal abnormalities were reported in about 40% of reported cases in the medical literature.

Since PDA is usually identified in infants, it is less common in adults, but it can have serious consequences, and is usually corrected surgically upon diagnosis.

Hypoplastic right heart syndrome is less common than hypoplastic left heart syndrome which occurs in 4 out of every 10,000 births. [3].

This rare anomaly requires prenatal diagnosis since it needs immediate and emergency treatment. Pregnant women whose pregnancy is complicated with this anomaly should be referred to a level 3 hospital with pediatric cardiology and pediatric cardiothoracic surgical team.[3]

It can be associated with aortic stenosis.

According to WHO classification there are 5 groups of PH, where Group I (pulmonary arterial hypertension) is further subdivided into Group I' and Group I" classes. The most recent WHO classification system (with adaptations from the more recent ESC/ERS guidelines shown in italics) can be summarized as follows:

WHO Group I – Pulmonary arterial hypertension (PAH)

- Idiopathic

- Heritable (BMPR2, ALK1, SMAD9, caveolin 1, KCNK3 mutations)

- Drug- and toxin-induced (e.g., methamphetamine use)

- Associated conditions:Connective tissue disease, HIV infection, Portal hypertension, Congenital heart diseases, Schistosomiasis

WHO Group I' – Pulmonary veno-occlusive disease (PVOD), pulmonary capillary hemangiomatosis (PCH)

- Idiopathic

- Heritable (EIF2AK4 mutations)

- Drugs, toxins and radiation-induced

- Associated conditions:connective tissue disease, HIV infection

WHO Group I" – Persistent pulmonary hypertension of the newborn

WHO Group II – Pulmonary hypertension secondary to left heart disease

- Left ventricular Systolic dysfunction

- Left ventricular Diastolic dysfunction

- Valvular heart disease

- Congenital/acquired left heart inflow/outflow tract obstruction and congenital cardiomyopathy

- Congenital/acquired pulmonary venous stenosis

WHO Group III – Pulmonary hypertension due to lung disease, chronic hypoxia

- Chronic obstructive pulmonary disease (COPD)

- Interstitial lung disease

- Mixed restrictive and obstructive pattern pulmonary diseases

- Sleep-disordered breathing

- Alveolar hypoventilation disorders

- Chronic exposure to high altitude

- Developmental abnormalities

WHO Group IV – chronic arterial obstruction

- Chronic thromboembolic pulmonary hypertension (CTEPH)

- Other pulmonary artery obstructions

- Angiosarcoma or other tumor within the blood vessels

- Arteritis

- Congenital pulmonary artery stenosis

- Parasitic infection (hydatidosis)

WHO Group V – Pulmonary hypertension with unclear or multifactorial mechanisms

- Hematologic diseases: chronic hemolytic anemia (including sickle cell disease)

- Systemic diseases: sarcoidosis, pulmonary Langerhans cell histiocytosis: lymphangioleiomyomatosis, neurofibromatosis, vasculitis

- Metabolic disorders: glycogen storage disease, Gaucher disease, thyroid diseases

- Others: pulmonary tumoral thrombotic microangiopathy, fibrosing mediastinitis, chronic kidney failure, segmental pulmonary hypertension (pulmonary hypertension restricted to one or more lobes of the lungs)

Due to its recent establishment as a diagnosis, and it being unclassified as a cardiomyopathy according to the WHO, it is not fully understood how common the condition is. Some reports suggest that it is in the order of 0.12 cases per 100,000. The low number of reported cases though is due to the lack of any large population studies into the disease and have been based primarily upon patients suffering from advanced heart failure. A similar situation occurred with hypertrophic cardiomyopathy, which was initially considered very rare; however is now thought to occur in one in every 500 people in the population.

Again due to this condition being established as a diagnosis recently, there are ongoing discussions as to its nature, and to various points such as the ratio of compacted to non-compacted at different age stages. However it is universally understood that non-compaction cardiomyopathy will be characterized anatomically by "deep trabeculations in the ventricular wall, which define recesses communicating with the main ventricular chamber. Major clinical correlates include systolic and diastolic dysfunction, associated at times with systemic embolic events."

The prognosis for pulmonary atresia varies for every child, if the condition is left uncorrected it may be fatal, but the prognosis has greatly improved over the years for those with pulmonary atresia. Some factors that affect how well the child does include how well the heart is beating, and the condition of the blood vessels that supply the heart. Most cases of pulmonary atresia can be helped with surgery, if the patient's right ventricle is exceptionally small, many surgeries will be needed in order to help stimulate normal circulation of blood to the heart.If uncorrected, babies with this type of congenital heart disease may only survive for the first few days of life. Many children with pulmonary atresia will go on to lead normal lives, though complications such as endocarditis, stroke and seizures are possible.

Persistent truncus arteriosus is a rare cardiac abnormality that has a prevalence of less than 1%.

The epidemiology of IPAH is about 125–150 deaths per year in the U.S., and worldwide the incidence is similar to the U.S. at 4 cases per million. However, in parts of Europe (France) indications are 6 cases per million of IPAH. Females have a higher incidence rate than males (2–9:1).

Other forms of PH are far more common. In systemic scleroderma, the incidence has been estimated to be 8 to 12% of all patients; in rheumatoid arthritis it is rare. However, in systemic lupus erythematosus it is 4 to 14%, and in sickle cell disease, it ranges from 20 to 40%. Up to 4% of people who suffer a pulmonary embolism go on to develop chronic thromboembolic disease including pulmonary hypertension. A small percentage of patients with COPD develop pulmonary hypertension with no other disease to explain the high pressure. On the other hand, obesity-hypoventilation syndrome is very commonly associated with right heart failure due to pulmonary hypertension.