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.

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.

Heart failure is usually associated with a volume overloaded state. Therefore, those with evidence of fluid overload should be treated initially with intravenous loop diuretics. In the absence of symptomatic low blood pressure intravenous nitroglycerin is often used in addition to diuretic therapy to improve congestive symptoms.

Volume status should still be adequately evaluated. Some heart failure patients on chronic diuretics can undergo excessive diuresis. In the case of diastolic dysfunction without systolic dysfunction, fluid resuscitation may, in fact, improve circulation by decreasing heart rate, which will allow the ventricles more time to fill. Even if the patient is edematous, fluid resuscitation may be the first line of treatment if the person's blood pressure is low. The person may, in fact, have too little fluid in their blood vessels, but if the low blood pressure is due to cardiogenic shock, the administration of additional fluid may worsen the heart failure and associated low blood pressure. If the person's circulatory volume is adequate but there is persistent evidence of inadequate end-organ perfusion, inotropes may be administered. In certain circumstances, a left ventricular assist device (LVAD) may be necessary.

Once the person is stabilized, attention can be turned to treating pulmonary edema to improve oxygenation. Intravenous furosemide is generally the first line. However, people on long-standing diuretic regimens can become tolerant, and dosages must be progressively increased. If high doses of furosemide are inadequate, boluses or continuous infusions of bumetanide may be preferred. These loop diuretics may be combined with thiazide diuretics such as oral metolazone or intravenous chlorothiazide for a synergistic effect. Intravenous preparations are physiologically preferred because of more predictable absorption due to intestinal edema, however, oral preparations can be significantly more cost effective.

In acute decompensated heart failure (ADHF), the immediate goal is to re-establish adequate perfusion and oxygen delivery to end organs. This entails ensuring that airway, breathing, and circulation are adequate. Immediate treatments usually involve some combination of vasodilators such as nitroglycerin, diuretics such as furosemide, and possibly noninvasive positive pressure ventilation (NIPPV).

Medications, while included in guidelines, have not been shown to improve survival to hospital discharge following out-of-hospital cardiac arrest. This includes the use of epinephrine, atropine, lidocaine, and amiodarone. Epinephrine is generally recommended every five minutes. Vasopressin overall does not improve or worsen outcomes compared to epinephrine.

Epinephrine does appear to improve short-term outcomes such as return of spontaneous circulation. Some of the lack of long-term benefit may be related to delays in epinephrine use. While evidence does not support its use in children guidelines state its use is reasonable. Lidocaine and amiodarone are also deemed reasonable in children with cardiac arrest who have a shockable rhythm. The general use of sodium bicarbonate or calcium is not recommended.

The 2010 guidelines from the American Heart Association no longer contain the recommendation for using atropine in pulseless electrical activity and asystole due to the lack of evidence for its use. Neither lidocaine nor amiodarone, in those who continue in ventricular tachycardia or ventricular fibrillation despite defibrillation, improves survival to hospital discharge but both equally improve survival to hospital admission.

Thrombolytics when used generally may cause harm but may be of benefit in those with a confirmed pulmonary embolism as the cause of arrest. Evidence for use of naloxone in those with cardiac arrest due to opioids is unclear but it may still be used. In those with cardiac arrest due to local anesthetic lipid emulsion may be used.

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.

Cooling adults after cardiac arrest who have a return of spontaneous circulation (ROSC) but no return of consciousness improves outcomes. This procedure is called targeted temperature management (previously known as therapeutic hypothermia). People are typically cooled for a 24-hour period, with a target temperature of . There are a number of methods used to lower the body temperature, such as applying ice packs or cold-water circulating pads directly to the body, or infusing cold saline. This is followed by gradual rewarming over the next 12 to 24 hrs.

Recent meta-analysis found that the use of therapeutic hypothermia after out-of-hospital cardiac arrest is associated with improved survival rates and better neurological outcomes.

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.

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.

The pain associated with myocardial infarction may be treated with nitroglycerin or morphine. Nitroglycerin (given under the tongue or intravenously) may improve the blood supply to the heart, and decrease the work the heart must do. It is an important part of therapy for its pain relief, despite there being no benefit to overall mortality. Morphine may also be used, and is effective for the pain associated with STEMI. The evidence for benefit from morphine on overall outcomes, however, is poor and there is some evidence of potential harm.

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

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.

Early detection and treatment are associated with higher rates of recovery and decreased morbidity and mortality.

Treatment for PPCM is similar to treatment for congestive heart failure. Conventional heart failure treatment includes the use of diuretics, beta blockers (B-B), and angiotensin-converting enzyme inhibitors (ACE-I) after delivery. Diuretics, preferably furosemide, help the body to get rid of excess water weight and also lower blood pressure. ACE-I and B-B improve blood circulation and contribute to the reversal of the immune system dysfunction associated with PPCM. If ACE-I is not well tolerated by the patient, it can be replaced by angiotensin receptor blockers (ARB). Hydralazine with nitrates may replace ACE-I in breastfeeding mothers or before delivery; however, evidence suggests that this course of treatment may not be as effective as ACE-I but beneficial when necessary.

If EF is less than 35%, anticoagulation is indicated, as there is a greater risk of developing left ventricular thrombi (blood clots). Sometimes implantation of a left ventricular assist device (LVAD) or even heart transplant also becomes necessary.

It is important that the patient receives regular follow-up care including frequent echocardiograms to monitor improvement or the lack thereof, particularly after changes of medical treatment regimes.

Patients who do not respond to initial treatment, defined as left ventricular EF remaining below 20% at two months or below 40% at three months with conventional treatment may merit further investigation, including cardiac magnetic resonance imaging (MRI), cardiac catheterization, and endomyocardial biopsy for special staining and for viral polymerase chain reaction (PCR) analysis. Antiviral therapy, immunoabsorption, intravenous gamma globulin, or other immunomodulation therapy may then be considered accordingly, but following a controlled research-type protocol.

Since no one knows for sure exactly when to discontinue treatment, even when recovery occurs quickly, it is still recommended that both ACE-I and B-B be continued for at least one year after diagnosis.

Generally, diastolic dysfunction is a chronic process. When this chronic condition is well tolerated by an individual, no specific treatment may be indicated. Rather, therapy should be directed at the root cause of the stiff left ventricle, with potential causes and aggravating factors like high blood pressure and diabetes treated appropriately. Conversely (as noted above), diastolic dysfunction tends to be better tolerated if the atrium is able to pump blood into the ventricles in a coordinated fashion. This does not occur in atrial fibrillation (AF), where there is no coordinated atrial activity and the left ventricle loses around 20% of its output. However, in chronic AF and in geriatric patients, AF is better tolerated and the cardiologist must choose between a stable AF at a lower rate and the risk of having an intermittent AF if he pretends to treat AF aggressively with all the thrombo-embolic risk it implies. In the same light, and also as noted above, if the atrial fibrillation persists and is resulting in a rapid heart rate, treatment must be given to slow down that rate. Usually digoxin maintains a stable rhythm. The use of a self-expanding device that attaches to the external surface of the left ventricle has been suggested, yet still awaits FDA approval. When the heart muscle squeezes, energy is loaded into the device, which absorbs the energy and releases it to the left ventricle in the diastolic phase. This helps retain muscle elasticity.

The role of specific treatments for diastolic dysfunction "per se" is as yet unclear. Diuretics can be useful, if these patients develop significant congestion, but patients must be monitored because they frequently develop hypotension.

Beta-blockers are the first-line therapy as they induce bradycardia and give time for ventricles to fill. There is some evidence that calcium channel blocker drugs may be of benefit in reducing ventricular stiffness in some cases (verapamil has the benefit lowering the heart rate). Likewise, treatment with angiotensin converting enzyme inhibitors, such as enalapril, ramipril, and many others, may be of benefit due to their effect on preventing ventricular remodeling but under control to avoid hypotension.

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.

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.

Rate control to a target heart rate of less than 110 beats per minute is recommended in most people. Lower heart rates may be recommended in those with left ventricular hypertrophy or reduced left ventricular function. Rate control is achieved with medications that work by increasing the degree of block at the level of the AV node, decreasing the number of impulses that conduct into the ventricles. This can be done with:

- Beta blockers (preferably the "cardioselective" beta blockers such as metoprolol, bisoprolol, or nebivolol)

- Non-dihydropyridine calcium channel blockers (e.g., diltiazem or verapamil)

- Cardiac glycosides (e.g., digoxin) – have less use, apart from in older people who are sedentary. They are not as effective as either beta blockers or calcium channel blockers.

In those with chronic disease either beta blockers or calcium channel blockers are recommended.

In addition to these agents, amiodarone has some AV node blocking effects (in particular when administered intravenously), and can be used in individuals when other agents are contraindicated or ineffective (particularly due to hypotension).

The prognosis for TIC after treatment of the underlying tachyarrhythmia is generally good. Studies show that left ventricular function often improves within 1 month of treatment of the tachyarrhythmia, and normalization of the left ventricular ejection fraction occurs in the majority of patients by 3 to 4 months. In some patients however, recovery of this function can take greater than 1 year or be incomplete. In addition, despite improvement in the left ventricular ejection fraction, studies have demonstrated that patients with prior TIC continue to demonstrate signs of negative cardiac remodeling including increased left ventricular end-systolic dimension, end-systolic volume, and end-diastolic volume. Additionally, recurrence of the tachyarrhythmia in patients with a history of TIC has been associated with a rapid decline in left ventricular ejection fraction and more severe cardiomyopathy that their prior presentation, which may be a result of the negative cardiac remodeling. There have also been cases of sudden death in patients with a history of TIC, which may be associated with worse baseline left ventricular dysfunction. Given these risks, routine monitoring with clinic visits, ECG, and echocardiography is recommended.

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

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.

Cardiac resuscitation guidelines (ACLS/BCLS) advise that Cardiopulmonary resuscitation should be initiated promptly to maintain cardiac output until the PEA can be corrected. The approach in treatment of PEA is to treat the underlying cause, if known (e.g. relieving a tension pneumothorax). Where an underlying cause for PEA cannot be determined and/or reversed, the treatment of pulseless electrical activity is similar to that for asystole. There is no evidence that external cardiac compression can increase cardiac output in any of the many scenarios of PEA, such as hemorrhage, in which impairment of cardiac filling is the underlying mechanism producing loss of a detectable pulse.

An intravenous or intraosseous line should be started to provide medications through. The mainstay of drug therapy for PEA is epinephrine (adrenaline) 1 mg every 3–5 minutes. Although previously the use of atropine was recommended in the treatment of PEA/asystole, this recommendation was withdrawn in 2010 by the American Heart Association due to lack of evidence for therapeutic benefit. Epinephrine too has a limited evidence base, and it is recommended on the basis of its mechanism of action.

Sodium bicarbonate 1meq per kilogram may be considered in this rhythm as well, although there is little evidence to support this practice. Its routine use is not recommended for patients in this context, except in special situations (e.g. preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdose).

All of these drugs should be administered along with appropriate CPR techniques. Defibrillators cannot be used to correct this rhythm, as the problem lies in the response of the myocardial tissue to electrical impulses.

For those who are stable with a monomorphic waveform the medications procainamide or sotalol may be used and are better than lidocaine. Evidence does not show that amiodarone is better than procainamide.

As a low magnesium level in the blood is a common cause of VT, magnesium sulfate can be given for torsades de pointes or if a low blood magnesium level is found/suspected.

Long-term anti-arrhythmic therapy may be indicated to prevent recurrence of VT. Beta-blockers and a number of class III anti-arrhythmics are commonly used, such as the beta-blockers carvedilol, metoprolol, and bisoprolol, and the Potassium-Channel-Blockers amiodarone, dronedarone,bretylium, sotalol, ibutilide, and dofetilide. Angiotensin-converting-eynsyme (ACE) inhibitors and aldostrone antatagonists are also sometimes used in this setting.

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.

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.