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.

A person's risk of developing heart failure is inversely related to their level of physical activity. Those who achieved at least 500 MET-minutes/week (the recommended minimum by U.S. guidelines) had lower heart failure risk than individuals who did not report exercising during their free time; the reduction in heart failure risk was even greater in those who engaged in higher levels of physical activity than the recommended minimum.

A number of medications may cause or worsen the disease. This includes NSAIDS, a number of anesthetic agents such as ketamine, thiazolidinediones, a number of cancer medications, salbutamol, and tamsulosin among others.

A 2015 SBU-report looking at non-chemical factors found an association for those:

- with mentally stressful work with a lack of control over their working situation — with an effort-reward imbalance

- who experience low social support at work; who experience injustice or experience insufficient opportunities for personal development; or those who experience job insecurity

- those who work night schedules; or have long working weeks

- those who are exposed to noise

Specifically the risk of stroke was also increased by exposure to ionizing radiation. Hypertension develops more often in those who experience job strain and who have shift-work. Differences between women and men in risk are small, however men risk suffering and dying of heart attacks or stroke twice as often as women during working life.

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

Hypertension or high blood pressure affects at least 4 billion people worldwide. Hypertensive heart disease is only one of several diseases attributable to high blood pressure. Other diseases caused by high blood pressure include ischemic heart disease, stroke, peripheral arterial disease, aneurysms and kidney disease. Hypertension increases the risk of heart failure by two or three-fold and probably accounts for about 25% of all cases of heart failure. In addition, hypertension precedes heart failure in 90% of cases, and the majority of heart failure in the elderly may be attributable to hypertension. Hypertensive heart disease was estimated to be responsible for 1.0 million deaths worldwide in 2004 (or approximately 1.7% of all deaths globally), and was ranked 13th in the leading global causes of death for all ages. A world map shows the estimated disability-adjusted life years per 100,000 inhabitants lost due to hypertensive heart disease in 2004.

A large number of causes of myocarditis have been identified, but often a cause cannot be found. In Europe and North America, viruses are common culprits. Worldwide, however, the most common cause is Chagas' disease, an illness endemic to Central and South America that is due to infection by the protozoan "Trypanosoma cruzi". Many of the causes listed below, particularly those involving protozoa, fungi, parasites, allergy, autoimmune disorders, and drugs are also causes of eosinophilic myocarditis.

The exact incidence of myocarditis is unknown. However, in series of routine autopsies, 1–9% of all patients had evidence of myocardial inflammation. In young adults, up to 20% of all cases of sudden death are due to myocarditis.

Among patients with HIV, myocarditis is the most common cardiac pathological finding at autopsy, with a prevalence of 50% or more.

There are more women than men with hypertension, and, although men develop hypertension earlier in life, hypertension in women is less well controlled. The consequences of high blood pressure in women are a major public health problem and hypertension is a more important contributory factor in heart attacks in women than men. Until recently women have been under-represented in clinical trials in hypertension and heart failure. Nevertheless, there is some evidence that the effectiveness of antihypertensive drugs differs between men and women and that treatment for heart failure may be less effective in women.

It is estimated that the incidence of PPCM in the United States is between 1 in 1300 to 4000 live births. While it can affect women of all races, it is more prevalent in some countries; for example, estimates suggest that PPCM occurs at rates of one in 1000 live births in South African Bantus, and as high as one in 300 in Haiti.

Some studies assert that PPCM may be slightly more prevalent among older women who have had higher numbers of liveborn children and among women of older and younger extremes of childbearing age. However, a quarter to a third of PPCM patients are young women who have given birth for the first time.

While the use of tocolytic agents or the development of preeclampsia (toxemia of pregnancy) and pregnancy-induced hypertension (PIH) may contribute to the worsening of heart failure, they do not cause PPCM; the majority of women have developed PPCM who neither received tocolytics nor had preeclampsia nor PIH.

In short, PPCM can occur in any woman of any racial background, at any age during reproductive years, and in any pregnancy.

HIV is a major cause of cardiomyopathy – in particular dilated cardiomyopathy. Dilated cardiomyopathy can be due to pericardial effusion or infective endocarditis, especially in intravenous drug users which are common in the HIV population. However, the most researched causes of cardiomyopathy are myocardial inflammation and infection caused by HIV-1. Toxoplasma gondii is the most common opportunistic infectious agent associated with myocarditis in AIDS. Coinfection with viruses (usually, coxsackievirus B3 and cytomegalovirus) seems to have an important affect in myocarditis. HIV-1 infection produces additional virus and cytokines such as TNF-α. This induces cardiomyocyte apoptosis. TNF-α causes a negative inotropic effect by interfering with the intracellular calcium ion concentrations. The intensity of the stains for TNF-α and iNOS of the myocardium was greater in patients with HIV associated cardiomyopathy, myocardial viral infection and was inversely correlated with CD4 count with antiretroviral therapy having no effect. Cardiac autoimmunity affects the pathogenesis of HIV-related heart disease as HIV-infected patients with dilated cardiomyopathy are more likely to have cardiac-specific autoantibodies than HIV-infected patients with healthy hearts and HIV-negative controls. Many patients with HIV have nutritional deficiencies which have been linked to left ventricular dysfunction. HIV-infected patients with encephalopathy are more likely to die of congestive heart failure than are those without encephalopathy. HAART has reduced the incidence of myocarditis thus reducing the prevalence of HIV-associated cardiomyopathy. Intravenous immunoglobulins (IVIGs) can also help patients with HIV-associated myocarditis.

Although in many cases no cause is apparent, dilated cardiomyopathy is probably the result of damage to the myocardium produced by a variety of toxic, metabolic, or infectious agents. It may be due to fibrous change of the myocardium from a previous myocardial infarction. Or, it may be the late sequelae of acute viral myocarditis, such as with Coxsackie B virus and other enteroviruses possibly mediated through an immunologic mechanism.

Other causes include:

- Chagas disease, due to "Trypanosoma cruzi". This is the most common infectious cause of dilated cardiomyopathy in Latin America

- Pregnancy. Dilated cardiomyopathy occurs late in gestation or several weeks to months postpartum as a peripartum cardiomyopathy. It is reversible in half of cases.

- Alcohol abuse (alcoholic cardiomyopathy)

- Nonalcoholic toxic insults include administration of certain chemotherapeutic agents, in particular doxorubicin (Adriamycin), and cobalt.

- Thyroid disease

- Inflammatory diseases such as sarcoidosis and connective tissue diseases

- Tachycardia-induced cardiomyopathy

- Muscular dystrophy

- Tuberculosis - 1 to 2% of TB cases.

- Autoimmune mechanisms

Recent studies have shown that those subjects with an extremely high occurrence (several thousands a day) of premature ventricular contractions (extrasystole) can develop dilated cardiomyopathy. In these cases, if the extrasystole are reduced or removed (for example, via ablation therapy) the cardiomyopathy usually regresses.

Although the disease is more common in African-Americans than in Caucasians, it may occur in any patient population.

Kidney failure is very common in patients suffering from congestive heart failure. It was shown that kidney failure complicates one-third of all admissions for heart failure, which is the leading cause of hospitalization in the United States among adults over 65 years old. These complications led to longer hospital stay, higher mortality, and greater chance for readmission. Another study found that 39% of patients in NYHA class 4 and 31% of patients in NYHA class 3 had severely impaired kidney function. Similarly, kidney failure can have deleterious effects on cardiovascular function. It was estimated that about 44% of deaths in patients with end-stage kidney failure (ESKF) are due to cardiovascular disease.

Cardiomegaly is a condition affecting the cardiovascular system, specifically the heart. This condition is strongly associated with congestive heart failure. Within the heart, the working fibers of the myocardial tissue increase in size. As the heart works harder the actin and myosin filaments experience less overlap which increases the size of the myocardial fibers. If there is less overlap of the protein filaments actin and myosin within the sarcomeres of muscle fibers, they will not be able to effectively pull on one another. If the heart tissue (walls of left and right ventricle) gets too big and stretches too far, then those filaments cannot effectively pull on one another to shorten the muscle fibers, thus impacting the heart's sliding filament mechanism. If fibers cannot shorten properly, and the heart cannot contract properly, then blood cannot be effectively pumped to the lungs to be re-oxygenated and to the body to deliver oxygen to the working tissues of the body.

Zidovudine is an example of a nucleoside analogue and has been shown to cause: myocarditis and dilated cardiomyopathy as well as an increase in total cholesterol, triglycerides, LDL, HDL and insulin resistance. Protease inhibitors are another group of drugs (e.g. ritonavir) and some of them can cause a range of problems such as: lipodystrophy, atherosclerosis, increase total cholesterol, triglyceride, HDL, LDL, and insulin resistance. Amphotericin B can cause dilated cardiomyopathy, hypertension and bradycardia whereas, Ganciclovir can cause ventricular tachycardia. Interferon-alpha can cause arrhythmia and myocardial infarction/ischemia.

Chronic stable heart failure may easily decompensate. This most commonly results from an intercurrent illness (such as pneumonia), myocardial infarction (a heart attack), abnormal heart rhythms (such as atrial fibrillation), uncontrolled high blood pressure, or the person's failure to maintain a fluid restriction, diet, or medication. Other well recognized precipitating factors include anemia and hyperthyroidism which place additional strain on the heart muscle. Excessive fluid or salt intake, and medication that causes fluid retention such as NSAIDs and thiazolidinediones, may also precipitate decompensation.

Acute myocardial infarction can precipitate acute decompensated heart failure and will necessitate emergent revascularization with thrombolytics, percutaneous coronary intervention, or coronary artery bypass graft.

The most recent studies indicate that with newer conventional heart failure treatment consisting of diuretics, ACE inhibitors and beta blockers, the survival rate is very high at 98% or better, and almost all PPCM patients improve with treatment. In the United States, over 50% of PPCM patients experience complete recovery of heart function (EF 55% or greater). Almost all recovered patients are eventually able to discontinue medications with no resulting relapse and have normal life expectancy.

It is a misconception that hope for recovery depends upon improvement or recovery within the first six to 12 months of diagnosis. Many women continue to improve or recover even years after diagnosis with continued medicinal treatment. Once fully recovered, if there is no subsequent pregnancy, the possibility of relapse or recurrence of heart failure is minimal.

Subsequent pregnancy should be avoided when left ventricular function has not recovered and the EF is lower than 55%. However, many women who have fully recovered from PPCM have gone on to have successful subsequent pregnancies. A significant study reports that the risk for recurrence of heart failure in recovered PPCM patients as a result of subsequent pregnancy is approximately 21% or better. The chance of relapse may be even smaller for those with normal contractile reserve as demonstrated by stress echocardiography. In any subsequent pregnancy, careful monitoring is necessary. Where relapse occurs, conventional treatment should be resumed, including hydralazine with nitrates plus beta-blockers during pregnancy, or ACE-inhibitors plus beta-blockers following pregnancy.

The true incidence of TIC is unclear. Some studies have noted the incidence of TIC in adults with irregular heart rhythms to range from 8% to 34%. Other studies of patients with atrial fibrillation and left ventricular dysfunction estimate that 25-50% of these study participants have some degree of TIC. TIC has been reported in all age groups.

Ultrafiltration can be used to remove fluids in people with ADHF associated with kidney failure. Studies have found that it decreases health care utilization at 90 days.

Autoimmune heart diseases are the effects of the body's own immune defense system mistaking cardiac antigens as foreign and attacking them leading to inflammation of the heart as a whole, or in parts. The commonest form of autoimmune heart disease is rheumatic heart disease or rheumatic fever.

The following risk factors have been associated with increased incidence of CRS.

- Older age

- Comorbid conditions (diabetes mellitus, uncontrolled hypertension, anemia)

- Drugs (anti-inflammatory agents, diuretics, ACE inhibitors, ARBs)

- History of heart failure or impaired left ventricular ejection fraction

- Prior myocardial infarction

- New York Heart Association (NYHA) functional class

- Elevated cardiac troponins

- Chronic kidney disease (reduced eGFR, elevated BUN, creatinine, or cystatin)

About 33 million people are affected by rheumatic heart disease with an additional 47 million having asymptomatic damage to their heart valves. As of 2010 globally it resulted in 345,000 deaths, down from 463,000 in 1990.

In Western countries, rheumatic fever has become fairly rare since the 1960s, probably due to the widespread use of antibiotics to treat streptococcus infections. While it has been far less common in the United States since the beginning of the 20th century, there have been a few outbreaks since the 1980s. Although the disease seldom occurs, it is serious and has a case-fatality rate of 2–5%.

Rheumatic fever primarily affects children between ages 5 and 17 years and occurs approximately 20 days after strep throat. In up to a third of cases, the underlying strep infection may not have caused any symptoms.

The rate of development of rheumatic fever in individuals with untreated strep infection is estimated to be 3%. The incidence of recurrence with a subsequent untreated infection is substantially greater (about 50%). The rate of development is far lower in individuals who have received antibiotic treatment. Persons who have suffered a case of rheumatic fever have a tendency to develop flare-ups with repeated strep infections.

The recurrence of rheumatic fever is relatively common in the absence of maintenance of low dose antibiotics, especially during the first three to five years after the first episode. Recurrent bouts of rheumatic fever can lead to valvular heart disease. Heart complications may be long-term and severe, particularly if valves are involved. In countries in Southeast-Asia, sub-saharan Africa, and Oceania, the percentage of people with rheumatic heart disease detected by listening to the heart was 2.9 per 1000 children and by echocardiography it was 12.9 per 1000 children.

Alcoholic cardiomyopathy is a disease in which the chronic long-term abuse of alcohol (i.e., ethanol) leads to heart failure. Alcoholic cardiomyopathy is a type of dilated cardiomyopathy. Due to the direct toxic effects of alcohol on heart muscle, the heart is unable to pump blood efficiently, leading to heart failure. It can affect other parts of the body if the heart failure is severe. It is most common in males between the ages of 35-50.

Treatment for alcoholic cardiomyopathy involves lifestyle changes, including complete abstinence from alcohol use, a low sodium diet, and fluid restriction, as well as medications. Medications may include ACE inhibitors, beta blockers, and diuretics which are commonly used in other forms of cardiomyopathy to reduce the strain on the heart. Persons with congestive heart failure may be considered for surgical insertion of an ICD or a pacemaker which can improve heart function. In cases where the heart failure is irreversible and worsening, heart transplant may be considered.

Treatment will possibly prevent the heart from further deterioration, and the cardiomyopathy is largely reversible if complete abstinence from alcohol is maintained.