The treatment for myocardial rupture is supportive in the immediate setting and surgical correction of the rupture, if feasible. A certain small percentage of individuals do not seek medical attention in the acute setting and survive to see the physician days or weeks later. In this setting, it may be reasonable to treat the rupture medically and delay or avoid surgery completely, depending on the individual's comorbid medical issues.

Dressler syndrome is best treated with high dose aspirin. In some resistant cases, corticosteroids can be used but are not preferred (avoided) in first month due to the high frequency of impaired ventricular healing leading to increased rate of ventricular rupture. NSAIDs though once used to treat Dressler syndrome, are less advocated and should be avoided in patients with ischemic heart disease. One NSAID in particular, indomethacin, can inhibit new collagen deposition thus impairing the healing process for the infarcted region. NSAIDS should only be used in cases refractory to aspirin. Heparin in Dressler syndrome should be avoided because it can lead to hemorrhage into the pericardial sac leading to tamponade. The only time heparin could be used with pericarditis is with coexisting acute MI in order to prevent further thrombus formation.

There are also surgical procedures for removal of a thrombus (thrombectomy).

Initial treatment given will usually be supportive in nature, for example administration of oxygen, and monitoring. There is little care that can be provided pre-hospital other than general treatment for shock. Some teams have performed an emergency thoracotomy to release clotting in the pericardium caused by a penetrating chest injury.

Prompt diagnosis and treatment is the key to survival with tamponade. Some pre-hospital providers will have facilities to provide pericardiocentesis, which can be life-saving. If the patient has already suffered a cardiac arrest, pericardiocentesis alone cannot ensure survival, and so rapid evacuation to a hospital is usually the more appropriate course of action.

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.

When discovered, hemopericardium is usually treated by pericardiocentesis, a procedure wherein a needle is used to remove the fluid from the pericardial sac. This procedure typically utilizes an 8-cm, 18-gauge needle that is inserted between the xiphoid process and the left costal margin until it enters the pericardial sac, when it can then be used to drain the fluid from the sac. A catheter is often left in the pericardium to continue draining any remaining fluid after the initial procedure. The catheter can be removed when the hemopericardium no longer persists. The underlying causes of the condition, such as over-prescription of anticoagulants, must be addressed as well so that the hemopericardium does not return.

While hemopericardium itself is not fatal, it may lead to cardiac tamponade, which can be deadly if not treated promptly. One study found that cardiac tamponade was fatal in 13.3% of cases in which it was not caused by a malignant disease.

After an AMI, people should be treated to prevent LVT formation. Aspirin plus an oral anticoagulant such as warfarin are suggested for individuals at risk for thromboembolic events. Anticoagulants are also shown to reduce the risk of embolisms when a thrombus is already formed. Heparin, an injectable, fast-acting anticoagulant, is effective in high doses for preventing LVT formation after AMI.

Initial management in hospital is by pericardiocentesis. This involves the insertion of a needle through the skin and into the pericardium and aspirating fluid under ultrasound guidance preferably. This can be done laterally through the intercostal spaces, usually the fifth, or as a subxiphoid approach. A left parasternal approach begins 3 to 5 cm left of the sternum to avoid the left internal mammary artery, in the 5th intercostal space. Often, a cannula is left in place during resuscitation following initial drainage so that the procedure can be performed again if the need arises. If facilities are available, an emergency pericardial window may be performed instead, during which the pericardium is cut open to allow fluid to drain. Following stabilization of the patient, surgery is provided to seal the source of the bleed and mend the pericardium.

In people following heart surgery the nurses monitor the amount of chest tube drainage. If the drainage volume drops off, and the blood pressure goes down, this can suggest tamponade due to chest tube clogging. In that case, the patient is taken back to the operating room for an emergency reoperation.

If aggressive treatment is offered immediately and no complications arise (shock, AMI or arrhythmia, heart failure, aneurysm, carditis, embolism, or rupture), or they are dealt with quickly and fully contained, then adequate survival is still a distinct possibility.

Some people live with this type of aneurysm for many years without any specific treatment. Treatment is limited to surgery (ventricular reduction) for this defect of the heart. However, surgery is not required in most cases but, limiting the patient's physical activity levels to lower the risk of making the aneurysm bigger is advised. Also ACE Inhibitors seem to prevent Left Ventricular remodeling and aneurysm formation.

Blood thinning agents may be given to help reduce the likelihood of blood thickening and clots forming, along with the use of drugs to correct the irregular rhythm of the heart (seen on the electrocardiogram)

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.

Hemopericardium has been reported to result from various afflictions including chest trauma, free wall rupture after a myocardial infarction, bleeding into the pericardial sac following a type A aortic dissection, and as a complication of invasive cardiac procedures. Acute leukemia has also been reported as a cause of the condition. Several cases of hemopericardium have also been reported as a side-effect of anticoagulants. Patients should be made aware of this fact when prescribed these drugs.

Depending on the type of cardiogenic shock, treatment involves infusion of fluids, or in shock refractory to fluids, inotropic medications. In case of an abnormal heart rhythm several anti-arrhythmic agents may be administered, e.g. adenosine.

Positive inotropic agents (such as dobutamine or milrinone), which enhance the heart's pumping capabilities, are used to improve the contractility and correct the low blood pressure. Should that not suffice an intra-aortic balloon pump (which reduces workload for the heart, and improves perfusion of the coronary arteries) or a left ventricular assist device (which augments the pump-function of the heart) can be considered. Finally, as a last resort, if the person is stable enough and otherwise qualifies, heart transplantation, or if not eligible an artificial heart, can be placed. These invasive measures are important tools- more than 50% of patients who do not die immediately due to cardiac arrest from a lethal abnormal heart rhythm and live to reach the hospital (who have usually suffered a severe acute myocardial infarction, which in itself still has a relatively high mortality rate), die within the first 24 hours. The mortality rate for those still living at time of admission who suffer complications (among others, cardiac arrest or further abnormal heart rhythms, heart failure, cardiac tamponade, a ruptured or dissecting aneurysm, or another heart attack) from cardiogenic shock is even worse around 85%, especially without drastic measures such as ventricular assist devices or transplantation.

Cardiogenic shock may be treated with intravenous dobutamine, which acts on β receptors of the heart leading to increased contractility and heart rate.

The prognosis of myocardial rupture is dependent on a number of factors, including which portion of the myocardium is involved in the rupture. In one case series, if myocardial rupture involved the free wall of the left ventricle, the mortality rate was 100.0%. The chances of survival rise dramatically if the patient: 1. has a witnessed initial event; 2. seeks early medical attention; 3. has an accurate diagnosis by the emergentologist; and 4. happens to be at a facility that has a cardiac surgery service (by whom a quick repair of the rupture can be attempted). Even if the individual survives the initial hemodynamic sequelae of the rupture, the 30‑day mortality is still significantly higher than if rupture did not occur.

Nitroglycerin can be used immediately to widen the coronary arteries and help increase blood flow to the heart. In addition, nitroglycerin causes peripheral venous and artery dilation reducing cardiac preload and afterload. These reductions allow for decreased stress on the heart and therefore lower the oxygen demand of the heart's muscle cells.

Antiplatelet drugs such as aspirin and clopidogrel can help reduce the progression of atherosclerotic plaque formation, as well as combining these with an anticoagulant such as a low molecular weight heparin.

For patients in acute heart failure, ACE inhibitors, angiotensin receptor blockers, and beta blockers, are considered mainstays of heart failure treatment. But use of beta blockers specifically for takotsubo cardiomyopathy is controversial, because they may confer no benefit.

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.

Treatment is varied depending upon the nature of the case. In severe cases, coronary artery bypass surgery is performed to redirect blood flow around the affected area. Drug-eluting stents and thrombolytic drug therapy are less invasive options for less severe cases.

The treatment of takotsubo cardiomyopathy is generally supportive in nature, for it is considered a transient disorder. Treatment is dependent on whether patients experience heart failure or acute hypotension and shock. In many individuals, left ventricular function normalizes within two months. Aspirin and other heart drugs also appear to help in the treatment of this disease, even in extreme cases. After the patient has been diagnosed, and myocardial infarction (heart attack) ruled out, the aspirin regimen may be discontinued, and treatment becomes that of supporting the patient.

While medical treatments are important to address the acute symptoms of Takotsubo cardiomyopathy, further treatment includes lifestyle changes. It is important that the individual stay physically healthy while learning and maintaining methods to manage stress, and to cope with future difficult situations.

Although the symptoms of Takotsubo cardiomyopathy usually go away on their own and the condition completely resolves itself within a few weeks, some serious complications can happen that must be treated. These most commonly include congestive heart failure and very low blood pressure, and less commonly include blood clotting in the apex of the left ventricle, irregular heart beat, and tearing of the heart wall.

The effectiveness and safety of ACE inhibitors and angiotensin receptor blockers acutely in ADHF have not been well studied, but are potentially harmful. A person should be stabilized before therapy with either of these medication classes is initiated. Individuals with poor kidney perfusion are especially at risk for kidney impairment inherent with these medications.

Beta-blockers are stopped or decreased in people with acutely decompensated heart failure and a low blood pressure. However, continuation of beta-blockers may be appropriate if the blood pressure is adequate.

Inotropes are indicated if low blood pressure ( SBP < 90 mmHg ) is present.

Opioids have traditionally been used in the treatment of the acute pulmonary edema that results from acute decompensated heart failure. A 2006 review, however, found little evidence to support this practice.

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.

Aortic dissection generally presents as a hypertensive emergency, and the prime consideration of medical management is strict blood pressure control. The target blood pressure should be a mean arterial pressure (MAP) of 60 to 75 mmHg, or the lowest blood pressure tolerated. Initial decreases should be by about 20%.

Another factor is to reduce the shear-force dP/dt (force of ejection of blood from the left ventricle). Long-term management of physical, emotional, and psychological stresses are important to controlling blood pressure.

Beta blockers are the first-line treatment for patients with acute and chronic aortic dissection. In acute dissection, fast-acting agents which can be given intravenously and have doses that are easier to adjust (such as esmolol, propranolol, or labetalol) are preferred. Vasodilators such as sodium nitroprusside can be considered for people with ongoing high blood pressure, but they should never be used alone, as they often stimulate a reflexive increase in the heart rate.

Calcium channel blockers can be used in the treatment of aortic dissection, particularly if a contraindication to the use of beta blockers exists. The calcium channel blockers typically used are verapamil and diltiazem, because of their combined vasodilator and negative inotropic effects.

If the individual has refractory hypertension (persistent hypertension on the maximum doses of three different classes of antihypertensive agents), an involvement of the renal arteries in the aortic dissection plane should be considered.

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.

Traumatic aortic rupture is treated with surgery. However, morbidity and mortality rates for surgical repair of the aorta for this condition are among the highest of any cardiovascular surgery. For example, surgery is associated with a high rate of paraplegia, because the spinal cord is very sensitive to ischemia (lack of blood supply), and the nerve tissue can be damaged or killed by the interruption of the blood supply during surgery.

A less invasive option for treatment is endovascular repair, which does not require open thoracotomy and can be safer for people with other injuries to organs.

Since high blood pressure could exacerbate an incomplete tear in the aorta or even separate it completely from the heart, which would almost inevitably kill the patient, hospital staff take measures to keep the blood pressure low. Such measures include giving pain medication, keeping the patient calm, and avoiding procedures that could cause gagging or vomiting. Beta blockers and vasodilators can be given to lower the blood pressure, and intravenous fluids that might normally be given are foregone to avoid raising it.

After return of heart function, there has been a moderately higher risk of death in the hospital when compared to MI patients without PVF. Whether this still holds true with the recent changes in treatment strategies of earlier hospital admission and immediate angioplasty with thrombus removal is unknown. PVF does not affect the long-term prognosis.

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.