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.

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

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)

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.

Warfarin and vitamin K antagonists are anticoagulants that can be taken orally to reduce thromboembolic occurrence. Where a more effective response is required, heparin can be given (by injection) concomitantly. As a side effect of any anticoagulant, the risk of bleeding is increased, so the international normalized ratio of blood is monitored. Self-monitoring and self-management are safe options for competent patients, though their practice varies. In Germany, about 20% of patients were self-managed while only 1% of U.S. patients did home self-testing (according to one 2012 study). Other medications such as direct thrombin inhibitors and direct Xa inhibitors are increasingly being used instead of warfarin.

Recommendations for those without cancer include anticoagulation (stopping further blood clots from forming) with dabigatran, rivaroxaban, apixaban, or edoxaban rather than warfarin or low molecular weight heparin (LMWH). For those with cancer LMWH is recommended. For initial treatment of VTE, fixed doses with LMWH may be more effective than adjusted doses of unfractionated heparin (UFH) in reducing blood clots. No differences in mortality, prevention of major bleeding, or preventing VTEs from recurring were observed between LMWH and UFH. No differences have been detected in the route of administration of UFH (subcutaneous or intravenous). LMWH is usually administered by a subcutaneous injection, and a persons blood clotting factors do not have to be monitored as closely as with UFH. People with cancer have a higher risk of experiencing reoccurring VTE episodes ("recurrent VTE"), despite taking preventative anticoagulation medication. These people should be given therapeutic doses of LMWH medication, either by switching from another anticoagulant or by taking a higher dose of LMWH.

For those with a small pulmonary embolism and few risk factors, no anticoagulation is needed. Anticoagulation is; however, recommended in those who do have risk factors. Thrombolysis is recommended in those with PEs that are causing low blood pressure.

Thrombolysis is the pharmacological destruction of blood clots by administering thrombolytic drugs including recombitant tissue plasminogen activator, which enhances the normal destruction of blood clots by the body's enzymes. This carries an increased risk of bleeding so is generally only used for specific situations (such as severe stroke or a massive pulmonary embolism).

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.

The main goals of treatment are to prevent circulatory instability and stroke. Rate or rhythm control are used to achieve the former, whereas anticoagulation is used to decrease the risk of the latter. If cardiovascularly unstable due to uncontrolled tachycardia, immediate cardioversion is indicated. Regular, moderate-intensity exercise is beneficial for people with AF.

Standard medical treatment consists of anticoagulants (blood thinners), diuretics, and oxygen. Lifelong anticoagulation is recommended, even after PEA. Routine inferior vena cava filter placement is not recommended.

In patients with non-operable CTEPH or persistent/recurrent PH after PEA, there is evidence for benefit from pulmonary vasodilator drug treatment. The microvascular disease component in CTEPH has provided the rationale for off-label use of drugs approved for PAH. Currently, only riociguat (a stimulator of soluble guanylate cyclase) is approved for treatment of adults with inoperable CTEPH or persistent or recurrent CTEPH after surgical treatment. Other drug trials are ongoing in patients with inoperable CTEPH, with macitentan recently proving efficacy and safety in MERIT

Evidence-based clinical guidelines were published in 2016 for the treatment of VTE.

Anticoagulation can be used to reduce the risk of stroke from AF. Anticoagulation is recommended in most people other than those at low risk of stroke or those at high risk of bleeding. The risk of falls and consequent bleeding in frail elderly people with atrial fibrillation should not be considered a barrier to initiating or continuing therapeutic anticoagulation since the risk of fall-related brain bleeding (intracranial hemorrhage) is low and the benefit of stroke prevention outweighs the risk of bleeding. Oral anticoagulation is underused in atrial fibrillation while aspirin is overused in many who should be treated with a novel oral anticoagulant or warfarin.

The risk of stroke from non-valvular AF can be estimated using the CHADS-VASc score. A 2014 AHA/ACC/HRS guideline said that for nonvalvular AF, anticoagulation is recommended if there is a score of 2 or more, not using anticoagulation or using aspirin may be considered if there is a score of 1, and not using anticoagulation is reasonable if there is a score of 0. In contrast, guidelines from the American College of Chest Physicians, Asia-Pacific Heart Rhythm Society, Canadian Cardiovascular Society, European Society of Cardiology, Japanese Circulation Society, Korean Heart Rhythm Society, and the National Institute for Health and Care Excellence recommend the use of novel oral anticoagulants or warfarin with a CHADS2VASC score of 1 over aspirin and some directly recommend against aspirin. Experts generally advocate for most people with atrial fibrillation with CHADS2VASC scores of 1 or more receiving anticoagulation though aspirin is sometimes used for people with a CHADS2VASC score of 1 (moderate risk for stroke). There is little evidence to support the idea that the use of aspirin significantly reduces the risk of stroke in people with atrial fibrillation. Furthermore, aspirin's major bleeding risk (including intracranial hemorrhage) is similar to that of warfarin and NOACs despite its inferior efficacy.

Anticoagulation can be achieved through a number of means including warfarin, heparin, dabigatran, rivaroxaban, edoxaban, and apixaban. A number of issues should be considered, including the cost of NOACs, risk of stroke, risk of falls, compliance, and speed of desired onset of anticoagulation.

For those with non-valvular atrial fibrillation, the NOACs (rivaroxaban, dabigatran, apixaban) are neither superior to nor worse than warfarin in preventing non-hemorrhagic stroke and systemic embolic events. They have a lower risk of intracranial bleeding compared to warfarin; however, dabigatran is associated with a higher risk of gastrointestinal bleeding.

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.

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.

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.

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.

In last decade, similar to myocardial infarction treatment, thrombolytic drugs were introduced in the therapy of cerebral infarction. The use of intravenous rtPA therapy can be advocated in patients who arrive to stroke unit and can be fully evaluated within 3 h of the onset.

If cerebral infarction is caused by a thrombus occluding blood flow to an artery supplying the brain, definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die. In increasing numbers of primary stroke centers, pharmacologic thrombolysis with the drug tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery.

Another intervention for acute cerebral ischaemia is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive thrombolytic drugs or for whom the drugs were ineffective, though no differences have been found between newer and older versions of the devices. The devices have only been tested on patients treated with mechanical clot embolectomy within eight hours of the onset of symptoms.

Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute cerebral ischaemia. In a systematic review of six uncontrolled, single-center trials, involving a total of 300 patients, of intra-cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical success (reduction to stenosis of <50%) ranged from 90-98%, and the rate of major peri-procedural complications ranged from 4-10%. The rates of restenosis and/or stroke following the treatment were also favorable. This data suggests that a large, randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this treatment.

If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after cerebral infarction. Carotid endarterectomy is also indicated to decrease the risk of cerebral infarction for symptomatic carotid stenosis (>70 to 80% reduction in diameter).

In tissue losses that are not immediately fatal, the best course of action is to make every effort to restore impairments through physical therapy, cognitive therapy, occupational therapy, speech therapy and exercise.

Decision making for patients with CTEPH can be complex and needs to be managed by CTEPH teams in expert centres. CTEPH teams comprise cardiologists and pulmonologists with specialist PH training, radiologists, experienced PEA surgeons with a significant caseload of CTEPH patients per year and physicians with percutaneous interventional expertise. Currently, there are three recognised targeted treatment options available: pulmonary endarterectomy (PEA), balloon pulmonary angioplasty (BPA) and pulmonary vasodilator drug treatment for inoperable patients.

Specialist imaging using either magnetic resonance or invasive PA is necessary to determine risks and benefits of interventional treatment with PEA or BPA.

The survival of PVF largely depends on the promptness of defibrillation. The success rate of prompt defibrillation during monitoring is currently higher than 95%. It is estimated that the success rate decreases by 10% for each additional minute of delay.

As previously stated, management of HFpEF is primarily dependent on the treatment of symptoms and exacerbating conditions. Currently treatment with ACE inhibitors, calcium channel blockers, beta blockers, and angiotensin receptor blockers are employed but do not have a proven benefit in HFpEF patients. Additionally, use of Diuretics or other therapies that can alter loading conditions or blood pressure should be used with caution. It is not recommended that patients be treated with phosphodiesterase-5-inhibitors or digoxin.

Antimineralocorticoid is currently recommended for patients with HFpEF who show elevated brain natriuretic peptide levels. Spironolactone is the first member of this drug class and the most frequently employed. Care should be taken to monitor serum potassium levels as well as kidney function, specifically glomerular filtration rate during treatment.

Beta blockers play a rather obscure role in HFpEF treatment but appear to play a beneficial role in patient management. There is currently a deficit of clinical evidence to support a particular benefit for HFpEF patients, with most evidence resulting from HFpEF patients' inclusion in broader heart failure trials. However, some evidence suggests that vasodilating beta blockers, such as nebivolol, can provide a benefit for patients with heart failure regardless of ejection fraction. Additionally, because of the chronotropic perturbation and diminished LV filling seen in HFpEF the bradycardic effect of beta blockers may enable improved filling, reduced myocardial oxygen demand and lowered blood pressure. However, this effect also can contribute to diminished response to exercise demands and can result in an excessive reduction in heart rate.

ACE inhibitors do not appear to improve morbidity or mortality associated with HFpEF alone. However, they are important in the management of hypertension, a significant player in the pathophysiology of HFpEF.

Angiotensin II receptor blocker treatment shows an improvement in diastolic dysfunction and hypertension that is comparable to other anti-hypertensive medication.

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.

Treatment of TIC involves treating both the tachyarrhythmia and the heart failure with the goal of adequate rate control or restoration of the normal heart rhythm (aka. normal sinus rhythm) to reverse the cardiomyopathy. The treatment of the tachyarrhythmia depends on the specific arrhythmia, but possible treatment modalities include rate control, rhythm control with antiarrhythmic agents and cardioversion, radiofrequency (RF) catheter ablation, or AV node ablation with permanent pacemaker implantation.

For TIC due to atrial fibrillation, rate control, rhythm control, and RF catheter ablation can be effective to control the tachyarrhythmia and improve left ventricular systolic function. For TIC due to atrial flutter, rate control is often difficult to achieve, and RF catheter ablation has a relatively high success rate with a low risk of complications. In patients with TIC due to other types of SVT, RF catheter ablation is recommended as a first-line treatment. In patients with TIC due to VT or PVCs, both antiarrhythmics and RF catheter ablation can be used. However, the options for antiarrhythmic agents are limited because certain agents can be proarrhythmic in the setting of myocardial dysfunction in TIC. Therefore, RF catheter ablation is often a safe and effective choice for treatment VT and PVCs causing TIC. In cases where other treatment strategies fail, AV node ablation with permanent pacemaker implantation can also be used to treat the tachyarrhythmia.

The treatment of heart failure commonly involves neurohormonal blockade with beta-blockers and angiotensin convertase inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) along with symptomatic management with diuretics. Beta-blockers and ACE inhibitors can inhibit and potentially reverse the negative cardiac remodeling, which refers to structural changes in the heart, that occurs in TIC. However, the need to continue these agents after treatment of the tacharrhythmia and resolution of left ventricular systolic dysfunction remains controversial.

Despite increasing incidence of HFpEF effective inroads to therapeutics have been largely unsuccessful. Currently, recommendations for treatment are directed at symptom relief and co-morbid conditions. Frequently this involves administration of diuretics to relieve complications associated with volume overload, such as leg swelling and high blood pressure.

Commonly encountered conditions that must be treated for and have independent recommendations for standard of care include atrial fibrillation, coronary artery disease, hypertension, and hyperlipidemia. There are particular factors unique to HFpEF that must be accounted for with therapy. Unfortunately, currently available randomized clinical trials addressing the therapeutic adventure for these conditions in HFpEF present conflicting or limited evidence.

Specific aspects of therapeutics should be avoided in HFpEF to prevent the deterioration of the condition. Considerations that are generalizable to heart failure include avoidance of a fast heart rate, elevations in blood pressure, development of ischemia, and atrial fibrillation. More specific to HFpEF include avoidance of preload reduction. As patients display normal ejection fraction but reduced cardiac output they are especially sensitive to changes in preloading and may rapidly display signs of output failure. This means administration of diuretics and vasodilators must be monitored carefully.

HFrEF and HFpEF represent distinct entities in terms of development and effective therapeutic management. Specifically cardiac resynchronization, administration of beta blockers and angiotensin converting enzyme inhibitors are applied to good effect in HFrEF but are largely ineffective at reducing morbidity and mortality in HFpEF. Many of these therapies are effective in reducing the extent of cardiac dilation and increasing ejection fraction in HFrEF patients. It is unsurprising they fail to effect improvement in HFpEF patients, given their un-dilated phenotype and relative normal ejection fraction. Understanding and targeting mechanisms unique to HFpEF are thus essential to the development of therapeutics.

Randomized studies on HFpEF patients have shown that exercise improves left ventricular diastolic function, the heart's ability to relax, and is associated with improved aerobic exercise capacity. The benefit patients seem to derive from exercise does not seem to be a direct cardiac effect but rather is due to changes in peripheral vasculature and skeletal muscle, which show abnormalities in HFpEF patients.

Patients should be regularly assessed to determine progression of the condition, response to interventions, and need for alteration of therapy. Ability to perform daily tasks, hemodynamic status, kidney function, electrolyte balance, and serum natriuretic peptide levels are important parameters. Behavioral management is important in these patients and it is recommended that individuals with HFpEF avoid alcohol, smoking, and high sodium intake.

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.

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.