It is recommended that blood pressure typically be reduced to less than 140/90 mmHg. The diastolic blood pressure however should not be lower than 60 mmHg. Beta blockers are recommended first line for this use.

There are a number of treatment options for coronary artery disease:

- Lifestyle changes

- Medical treatment – drugs (e.g., cholesterol lowering medications, beta-blockers, nitroglycerin, calcium channel blockers, etc.);

- Coronary interventions as angioplasty and coronary stent;

- Coronary artery bypass grafting (CABG)

Cardiovascular disease is treatable with initial treatment primarily focused on diet and lifestyle interventions. Influenza may make heart attacks and strokes more likely and therefore influenza vaccination may decrease the chance of cardiovascular events and death in people with heart disease.

Proper CVD management necessitates a focus on MI and stroke cases due to their combined high mortality rate, keeping in mind the cost-effectiveness of any intervention, especially in developing countries with low or middle income levels. Regarding MI, strategies using aspirin, atenolol, streptokinase or tissue plasminogen activator have been compared for quality-adjusted life-year (QALY) in regions of low and middle income. The costs for a single QALY for aspirin, atenolol, streptokinase, and t-PA were $25, $630–$730, and $16,000, respectively. Aspirin, ACE inhibitors, beta blockers, and statins used together for secondary CVD prevention in the same regions showed single QALY costs of $300–400.

While a healthy diet is beneficial, the effect of antioxidant supplementation (vitamin E, vitamin C, etc.) or vitamins has not been shown to protect against cardiovascular disease and in some cases may possibly result in harm. Mineral supplements have also not been found to be useful. Niacin, a type of vitamin B3, may be an exception with a modest decrease in the risk of cardiovascular events in those at high risk. Magnesium supplementation lowers high blood pressure in a dose dependent manner. Magnesium therapy is recommended for people with ventricular arrhythmia associated with torsades de pointes who present with long QT syndrome as well as for the treatment of people with digoxin intoxication-induced arrhythmias. There is no evidence to support omega-3 fatty acid supplementation.

Coronary ischemia can be treated but not cured.

By changing lifestyle, further blockages can be prevented. A change in lifestyle, mixed with prescribed medication, can improve health.

Following a heart attack, nitrates, when taken for two days, and ACE-inhibitors decrease the risk of death. Other medications include:

Aspirin is continued indefinitely, as well as another antiplatelet agent such as clopidogrel or ticagrelor ("dual antiplatelet therapy" or DAPT) for up to twelve months. If someone has another medical condition that requires anticoagulation (e.g. with warfarin) this may need to be adjusted based on risk of further cardiac events as well as bleeding risk. In those who have had a stent, more than 12 months of clopidogrel plus aspirin does not affect the risk of death.

Beta blocker therapy such as metoprolol or carvedilol is recommended to be started within 24 hours, provided there is no acute heart failure or heart block. The dose should be increased to the highest tolerated. Contrary to what was long believed, the use of beta blockers does not appear to affect the risk of death, possibly because other treatments for MI have improved. When beta blocker medication is given within the first 24–72 hours of a STEMI no lives are saved. However, 1 in 200 people were prevented from a repeat heart attack, and another 1 in 200 from having an abnormal heart rhythm. Additionally, for 1 in 91 the medication causes a temporary decrease in the heart's ability to pump blood.

ACE inhibitor therapy should be started within 24 hours, and continued indefinitely at the highest tolerated dose. This is provided there is no evidence of worsening kidney failure, high potassium, low blood pressure, or known narrowing of the renal arteries. Those who cannot tolerate ACE inhibitors may be treated with an angiotensin II receptor antagonist.

Statin therapy has been shown to reduce mortality and subsequent cardiac events, and should be commenced with the aim of lowering LDL cholesterol. Other medications, such as ezetimibe, may also be added with this goal in mind.

Aldosterone antagonists (spironolactone or eplerenone) may be used if there is evidence of left ventricular dysfunction after an MI, ideally after beginning treatment with an ACE inhibitor.

First-line therapy for people with heart failure due to reduced systolic function should include angiotensin-converting enzyme (ACE) inhibitors (ACE-I) or angiotensin receptor blockers (ARBs) if the person develops a long term cough as a side effect of the ACE-I. Use of medicines from this class is associated with improved survival and quality of life in people with heart failure.

Beta-adrenergic blocking agents (beta blockers) also form part of the first line of treatment, adding to the improvement in symptoms and mortality provided by ACE-I/ARB. The mortality benefits of beta blockers in people with systolic dysfunction who also have atrial fibrillation (AF) is more limited than in those who do not have AF. If the ejection fraction is not diminished (HFpEF), the benefits of beta blockers are more modest; a decrease in mortality has been observed but reduction in hospital admission for uncontrolled symptoms has not been observed.

In people who are intolerant of ACE-I and ARBs or who have significant kidney dysfunction, the use of combined hydralazine and a long-acting nitrate, such as isosorbide dinitrate, is an effective alternate strategy. This regimen has been shown to reduce mortality in people with moderate heart failure. It is especially beneficial in African-Americans (AA). In AAs who are symptomatic, hydralazine and isosorbide dinitrate (H+I) can be added to ACE-I or ARBs.

In people with markedly reduced ejection fraction, the use of an aldosterone antagonist, in addition to beta blockers and ACE-I, can improve symptoms and reduce mortality.

Second-line medications for CHF do not confer a mortality benefit. Digoxin is one such medication. Its narrow therapeutic window, a high degree of toxicity, and the failure of multiple trials to show a mortality benefit have reduced its role in clinical practice. It is now used in only a small number of people with refractory symptoms, who are in atrial fibrillation and/or who have chronic low blood pressure.

Diuretics have been a mainstay of treatment for treatment of fluid accumulation, and include diuretics classes such as loop diuretics, thiazide-like diuretic, and potassium-sparing diuretic. Although widely used, evidence on their efficacy and safety is limited, with the exception of mineralocorticoid antagonists such as spironolactone. Mineralocorticoid antagonists in those under 75 years old appear to decrease the risk of death. A recent Cochrane review found that in small studies, the use of diuretics appeared to have improved mortality in individuals with heart failure. However, the extent to which these results can be extrapolated to a general population is unclear due to the small number of participants in the cited studies.

Anemia is an independent factor in mortality in people with chronic heart failure. The treatment of anemia significantly improves quality of life for those with heart failure, often with a reduction in severity of the NYHA classification, and also improves mortality rates. The latest European guidelines (2012) recommend screening for iron-deficient anemia and treating with parenteral iron if anemia is found.

The decision to anticoagulate people with HF, typically with left ventricular ejection fractions <35% is debated, but generally, people with coexisting atrial fibrillation, a prior embolic event, or conditions which increase the risk of an embolic event such as amyloidosis, left ventricular noncompaction, familial dilated cardiomyopathy, or a thromboembolic event in a first-degree relative.

Aggressive risk factor modification is required for effective treatment of microvascular angina where exercise plays a major role. Several other treatment strategies including b-blockers, angiotensin-converting enzyme inhibitors, ranolazine, l-arginine, statin drugs and potentially estrogen replacement therapy have been shown to relieve anginal symptoms as well as improve vascular function. Nitrates may be effective for symptom relief. Further studies are required to determine whether specific treatments are associated with improved survival as well as decreased symptoms.

The most specific medicine to treat angina is nitroglycerin. It is a potent vasodilator that decreases myocardial oxygen demand by decreasing the heart's workload. Beta blockers and calcium channel blockers act to decrease the heart's workload, and thus its requirement for oxygen. Nitroglycerin should not be given if certain inhibitors such as sildenafil, tadalafil, or vardenafil have been taken within the previous 12 hours as the combination of the two could cause a serious drop in blood pressure. Treatments for angina are balloon angioplasty, in which the balloon is inserted at the end of a catheter and inflated to widen the arterial lumen. Stents to maintain the arterial widening are often used at the same time. Coronary bypass surgery involves bypassing constricted arteries with venous grafts. This is much more invasive than angioplasty.

The main goals of treatment in angina pectoris are relief of symptoms, slowing progression of the disease, and reduction of future events, especially heart attacks and death. Beta blockers (e.g., carvedilol, propranolol, atenolol) have a large body of evidence in morbidity and mortality benefits (fewer symptoms, less disability and longer life) and short-acting nitroglycerin medications have been used since 1879 for symptomatic relief of angina. Calcium channel blockers (such as nifedipine (Adalat) and amlodipine), isosorbide mononitrate and nicorandil are vasodilators commonly used in chronic stable angina. A new therapeutic class, called If inhibitor, has recently been made available: Ivabradine provides pure heart rate reduction leading to major anti-ischemic and antianginal efficacy. ACE inhibitors are also vasodilators with both symptomatic and prognostic benefit. Statins are the most frequently used lipid/cholesterol modifiers, which probably also stabilize existing atheromatous plaque. Low-dose aspirin decreases the risk of heart attack in patients with chronic stable angina, and was part of standard treatment. However, in patients without established cardiovascular disease, the increase in hemorrhagic stroke and gastrointestinal bleeding offsets any benefits and it is no longer advised unless the risk of myocardial infarction is very high.

Exercise is also a very good long-term treatment for the angina (but only particular regimens - gentle and sustained exercise rather than intense short bursts), probably working by complex mechanisms such as improving blood pressure and promoting coronary artery collateralisation.

Though sometimes used by patients, evidence does not support the use of Traditional Chinese Herbal Products (THCP) for angina

Identifying and treating risk factors for further coronary heart disease is a priority in patients with angina. This means testing for elevated cholesterol and other fats in the blood, diabetes and hypertension (high blood pressure), and encouraging smoking cessation and weight optimization.

The calcium channel blocker nifedipine prolongs cardiovascular event- and procedure-free survival in patients with coronary artery disease. New overt heart failures were reduced by 29% compared to placebo; however, the mortality rate difference between the two groups was statistically insignificant.

If PCI cannot be performed within 90 to 120 minutes in STEMI then fibrinolysis, preferably within 30 minutes of arrival to hospital, is recommended. If a person has had symptoms for 12 to 24 hours evidence for effectiveness of thrombolysis is less and if they have had symptoms for more than 24 hours it is not recommended. Thrombolysis involves the administration of medication that activates the enzymes that normally dissolve blood clots. These medications include tissue plasminogen activator, reteplase, streptokinase, and tenecteplase. Thrombolysis is not recommended in a number of situations, particularly when associated with a high risk of bleeding or the potential for problematic bleeding, such as active bleeding, past strokes or bleeds into the brain, or severe hypertension. Situations in which thrombolysis may be considered, but with caution, include recent surgery, use of anticoagulants, pregnancy, and proclivity to bleeding. Major risks of thrombolysis are major bleeding and intracranial bleeding. Pre-hospital thrombolysis reduces time to thrombolytic treatment, based on studies conducted in higher income countries, however it is unclear whether this has an impact on mortality rates.

At present, there is no effective specific treatment available for diabetic cardiomyopathy. Treatment centers around intense glycemic control through diet, oral hypoglycemics and frequently insulin and management of heart failure symptoms. There is a clear correlation between increased glycemia and risk of developing diabetic cardiomyopathy, therefore, keeping glucose concentrations as controlled as possible is paramount. Thiazolidinediones are not recommended in patients with NYHA Class III or IV heart failure secondary to fluid retention.

As with most other heart diseases, ACE inhibitors can also be administered. An analysis of major clinical trials shows that diabetic patients with heart failure benefit from such a therapy to a similar degree as non-diabetics. Similarly, beta blockers are also common in the treatment of heart failure concurrently with ACE inhibitors.

Restoring adequate blood flow to the heart muscle in people with heart failure and significant coronary artery disease is strongly associated with improved survival, some research showing up to 75% survival rates over 5 years. A stem cell study indicated that using autologous cardiac stem cells as a regenerative approach for the human heart (after a heart attack) has great potential.

American Heart Association practice guidelines indicate (ICD) implantable cardioverter-defibrillator use in those with ischemic cardiomyopathy (40 days post-MI) that are (NYHA) New York Heart Association functional class I. LVEF of >30% is often used to differentiate primary from ischemic cardiomyopathy, and a prognostic indicator. At the same time, people who undergo ventricular restoration on top of coronary artery bypass show improved postoperative ejection fraction as compared to those treated with only coronary artery bypass surgery. Severe cases are treated with heart transplantation.

By increasing physical activity, it is possible to manage body weight, reduce blood pressure, and relieve stress.

The Center for Disease Control recommends 30 minutes of physical activity a day.

Instead of 30 minutes a day at one time, short bursts of physical activity for 8–10 minutes three times a day are also suitable. Exercising this way can reduce the risk of getting heart disease or coronary ischemia, if it is performed at moderate intensity.

Treatment focuses on improving the symptoms and preventing the progression of the disease. Reversible causes of the heart failure also need to be addressed (e.g. infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, hypertension). Treatments include lifestyle and pharmacological modalities, and occasionally various forms of device therapy and rarely cardiac transplantation.

The medical care of patients with hypertensive heart disease falls under 2 categories—

- Treatment of hypertension

- Prevention (and, if present, treatment) of heart failure or other cardiovascular disease

Because there are no symptoms with high blood pressure, people can have the condition without knowing it. Diagnosing high blood pressure early can help prevent heart disease, stroke, eye problems, and chronic kidney disease.

The risk of cardiovascular disease and death can be reduced by lifestyle modifications, including dietary advice, promotion of weight loss and regular aerobic exercise, moderation of alcohol intake and cessation of smoking. Drug treatment may also be needed to control the hypertension and reduce the risk of cardiovascular disease, manage the heart failure, or control cardiac arrhythmias. Patients with hypertensive heart disease should avoid taking over the counter nonsteroidal anti-inflammatory drugs (NSAIDs), or cough suppressants, and decongestants containing sympathomimetics, unless otherwise advised by their physician as these can exacerbate hypertension and heart failure.

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.

One of the most important features differentiating ischemic cardiomyopathy from the other forms of cardiomyopathy is the shortened, or worsened all-cause mortality in patients with ischemic cardiomyopathy. According to several studies, coronary artery bypass graft surgery has a survival advantage over medical therapy (for ischemic cardiomyopathy) across varied follow-ups.

Medical management of patients with CRS is often challenging as focus on treatment of one organ may have worsening outcome on the other. It is known that many of the medications used to treat HF may worsen kidney function. In addition, many trials on HF excluded patients with advanced kidney dysfunction. Therefore, our understanding of CRS management is still limited to this date.

Diuretics

ACEI, ARB, renin inhibitors, aldosterone inhibitors

Natriuretic peptides

Vasopressin antagonists

Adenosine antagonists

Ultrafiltration

Inotropes

Many factors influence the time course and extent of remodeling, including the severity of the injury, secondary events (recurrent ischemia or infarction), neurohormonal activation, genetic factors and gene expression, and treatment. Medications may attenuate remodeling. Angiotensin-converting enzyme (ACE) inhibitors have been consistently shown to decrease remodeling in animal models or transmural infarction and chronic pressure overload. Clinical trials have shown that ACE inhibitor therapy after myocardial infarction leads to improved myocardial performance, improved ejection fraction, and decreased mortality compared to patients treated with placebo. Likewise, inhibition of aldosterone, either directly or indirectly, leads to improvement in remodeling. Carvedilol, a 3rd generation beta blocker, may actually reverse the remodeling process by reducing left ventricular volumes and improving systolic function. Early correction of congenital heart defects, if appropriate, may prevent remodeling, as will treatment of chronic hypertension or valvular heart disease. Often, reverse remodeling, or improvement in left ventricular function, will also be seen.

Artificial pacemakers may be used in patients with intraventricular conduction delay, and implantable cardioverter-defibrillators in those at risk of arrhythmia. These forms of treatment have been shown to prevent sudden cardiac death, improve symptoms, and reduce hospitalization in patients with systolic heart failure.

Drug therapy can slow down progression and in some cases even improve the heart condition. Standard therapy may include salt restriction, ACE inhibitors, diuretics, and beta blockers. Anticoagulants may also be used for antithrombotic therapy. There is some evidence for the benefits of coenzyme Q10 in treating heart failure.

Initial therapy of acute decompensated heart failure usually includes some combination of a vasodilator such as nitroglycerin, a loop diuretic such as furosemide, and non-invasive positive pressure ventilation (NIPPV).

Even if symptoms of heart failure are not present, medications can be used to treat the symptoms that are being experienced. These medicines work to control these symptoms as well as treat other health problems that might be present. They can work to improve the quality of life, slow down the progression of heart failure and reduce the risk for other complications that can occur due to heart failure. It is very important to take proper medicines exactly as prescribed by the physician.

A number of different medications are required for people who are experiencing heart failure. Common types of medications that are prescribed for heart failure patients include ACE inhibitors, vasodilators, beta blockers, aspirin, calcium channel blockers, and cholesterol lowering medications such as statins. Depending on the type of damage a patient has suffered and the underlying cause of the heart failure, any of these drug classes or a combination of them can be prescribed. Patients with heart pumping problems will use a different medication combination than those who are experiencing problems with the heart's ability to fill properly during diastole. Potentially dangerous drug interactions can occur when different drugs mix together and work against each other.

Nitrates such as nitroglycerin are often used as part of the initial therapy for ADHF.

Another option is nesiritide, although it should only be considered if conventional therapy has been ineffective or contraindicated as it is much more expensive than nitroglycerine and has not been shown to be of any greater benefit.

The treatment for cor pulmonale can include the following: antibiotics, expectorants, oxygen therapy, diuretics, digitalis, vasodilators, and anticoagulants. Some studies have indicated that Shenmai injection with conventional treatment is safe and effective for cor pulmonale (chronic).

Treatment requires diuretics (to decrease strain on the heart). Oxygen is often required to resolve the shortness of breath. Additionally, oxygen to the lungs also helps relax the blood vessels and eases right heart failure. When wheezing is present, the majority of individuals require a bronchodilator. A variety of drugs have been developed to relax the blood vessels in the lung, calcium channel blockers are used but only work in few cases and according to NICE are not recommended for use at all.

Anticoagulants are used when venous thromboembolism is present. Venesection is used in severe secondary polycythaemia (because of hypoxia), which improves symptoms though survival rate has not been proven to increase.Finally, transplantation of single/double lung in extreme cases of cor pulmonale is also an option.