The left side of the heart is responsible for receiving oxygen-rich blood from the lungs and pumping it forward to the systemic circulation (the rest of the body except for the pulmonary circulation). Failure of the left side of the heart causes blood to back up (be congested) into the lungs, causing respiratory symptoms as well as fatigue due to insufficient supply of oxygenated blood. Common respiratory signs are increased rate of breathing and increased "work" of breathing (non-specific signs of respiratory distress). Rales or crackles, heard initially in the lung bases, and when severe, throughout the lung fields suggest the development of pulmonary edema (fluid in the alveoli). Cyanosis which suggests severe low blood oxygen, is a late sign of extremely severe pulmonary edema.

Additional signs indicating left ventricular failure include a laterally displaced apex beat (which occurs if the heart is enlarged) and a gallop rhythm (additional heart sounds) may be heard as a marker of increased blood flow or increased intra-cardiac pressure. Heart murmurs may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure.

"Backward" failure of the left ventricle causes congestion of the lungs' blood vessels, and so the symptoms are predominantly respiratory in nature. Backward failure can be subdivided into the failure of the left atrium, the left ventricle or both within the left circuit. The patient will have dyspnea (shortness of breath) on exertion and in severe cases, dyspnea at rest. Increasing breathlessness on lying flat, called orthopnea, occurs. It is often measured in the number of pillows required to lie comfortably, and in orthopnea, the patient may resort to sleeping while sitting up. Another symptom of heart failure is paroxysmal nocturnal dyspnea: a sudden nighttime attack of severe breathlessness, usually several hours after going to sleep. Easy fatigability and exercise intolerance are also common complaints related to respiratory compromise.

"Cardiac asthma" or wheezing may occur.

Compromise of left ventricular "forward" function may result in symptoms of poor systemic circulation such as dizziness, confusion and cool extremities at rest.

Heart failure symptoms are traditionally and somewhat arbitrarily divided into "left" and "right" sided, recognizing that the left and right ventricles of the heart supply different portions of the circulation. However, heart failure is not exclusively "backward failure" (in the part of the circulation which drains to the ventricle).

There are several other exceptions to a simple left-right division of heart failure symptoms. Additionally, the most common cause of right-sided heart failure is left-sided heart failure. The result is that patients commonly present with both sets of signs and symptoms.

The symptoms and signs of hypertensive heart disease will depend on whether or not it is accompanied by heart failure. In the absence of heart failure, hypertension, with or without enlargement of the heart (left ventricular hypertrophy) is usually symptomless.

Symptoms, signs and consequences of Congestive heart failure can include:

- Fatigue

- Irregular pulse or palpitations

- Swelling of feet and ankles

- Weight gain

- Nausea

- Shortness of breath

- Difficulty sleeping flat in bed (orthopnea)

- Bloating and abdominal pain

- Greater need to urinate at night

- An enlarged heart (cardiomegaly)

- Left ventricular hypertrophy and left ventricular remodeling

- Diminished coronary flow reserve and silent myocardial ischemia

- Coronary heart disease and accelerated atherosclerosis

- Heart Failure With Normal Left Ventricular Ejection Fraction (HFNEF), often termed diastolic heart failure

- Atrial fibrillation, other cardiac arrhythmias, or sudden cardiac death

Heart failure can develop insidiously over time or patients can present acutely with acute heart failure or acute decompensated heart failure and pulmonary edema due to sudden failure of pump function of the heart. Sudden failure can be precipitated by a variety of causes, including myocardial ischemia, marked increases in blood pressure, or cardiac arrhythmias.

For many people cardiomegaly is asymptomatic. For others, if the enlarged heart begins to affect the body's ability to pump blood effectively, then symptoms associated with congestive heart failure may arise.

- Heart palpitations – irregular beating of the heart, usually associated with a valve issue inside the heart.

- Severe shortness of breath (especially when physically active) – irregularly unable to catch one's breath.

- Chest pain

- Fatigue

- Swelling in legs

- Increased abdominal girth

- Weight gain

- Edema – swelling

- Fainting

Other conditions can share features with hypertensive heart disease and need to be considered in the differential diagnosis. For example:

- Coronary artery disease or ischemic heart disease due to atherosclerosis

- Hypertrophic cardiomyopathy

- Left ventricular hypertrophy in athletes

- Congestive heart failure or heart failure with normal ejection fraction due to other causes

- Atrial fibrillation or other disorders of cardiac rhythm due to other causes

- Sleep apnea

Cardiac arrest is preceded by no warning symptoms in approximately 50% of people. For those who do, they have non specific symptoms such as, new or worsening chest pain, fatigue, blackouts, dizziness, shortness of breath, weakness, and vomiting.

When the arrest occurs, the most obvious sign of its occurrence will be the lack of a palpable pulse in the person experiencing it (since the heart has ceased to contract, the usual indications of its contraction such as a pulse will no longer be detectable). Certain types of prompt intervention can often reverse a cardiac arrest, but without such intervention the event will almost always lead to death. In certain cases, it is an expected outcome of a serious illness where death is expected.

Also, as a result of inadequate blood flow to the brain (cerebral perfusion), the patient will quickly become unconscious and will have stopped breathing. The main diagnostic criterion to diagnose a cardiac arrest (as opposed to respiratory arrest which shares many of the same features) is lack of circulation; however, there are a number of ways of determining this. Near-death experiences are reported by 10–20% of people who survived cardiac arrest.

Cardiomegaly is a medical condition in which the heart is enlarged. It is more commonly referred to as an enlarged heart. The causes of cardiomegaly may vary. Many times this condition results from high blood pressure (hypertension) or coronary artery disease. An enlarged heart may not pump blood effectively, resulting in congestive heart failure. Cardiomegaly may improve over time, but many people with an enlarged heart need lifelong treatment with medications. Having an immediate family member who has or had cardiomegaly may indicate that a person is more susceptible to getting this condition. Cardiomegaly is not a disease but rather a condition that can result from a host of other diseases such as obesity or coronary artery disease. Recent studies suggest that cardiomegaly is associated with a higher risk of sudden cardiac death (SCD).

Signs and symptoms presented by the occurrence of alcoholic cardiomyopathy are the result of the heart failing and usually occur after the disease has progressed to an advanced stage. Therefore, the symptoms have a lot in common with other forms of cardiomyopathy. These symptoms can include the following:

- Ankle, feet, and leg swelling (edema)

- Overall swelling

- Loss of appetite

- Shortness of breath (dyspnea), especially with activity

- Breathing difficulty while lying down

- Fatigue, weakness, faintness

- Decreased alertness or concentration

- Cough containing mucus, or pink, frothy material

- Decreased urine output (oliguria)

- Need to urinate at night (nocturia)

- Heart palpitations (irregular heart beat)

- Rapid pulse (tachycardia)

Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) occur when the heart abruptly begins to beat in an abnormal or irregular rhythm (arrhythmia). Without organized electrical activity in the heart muscle, there is no consistent contraction of the ventricles, which results in the heart's inability to generate an adequate cardiac output (forward pumping of blood from heart to rest of the body). There are many different types of arrhythmias, but the ones most frequently recorded in SCA and SCD are ventricular tachycardia (VT) or ventricular fibrillation (VF).

Sudden cardiac arrest can result from cardiac and non-cardiac causes including the following:

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

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

Dilated cardiomyopathy develops insidiously, and may not initially cause symptoms significant enough to impact on quality of life. Nevertheless, many people experience significant symptoms. These might include:

- Shortness of breath

- Syncope (fainting)

- Angina, but only in the presence of ischemic heart disease

A person suffering from dilated cardiomyopathy may have an enlarged heart, with pulmonary edema and an elevated jugular venous pressure and a low pulse pressure. Signs of mitral and tricuspid regurgitation may be present.

Difficulty breathing, a cardinal symptom of left ventricular failure, may manifest with progressively increasing severity as the following:

- Difficulty breathing with physical activity (exertional dyspnea)

- Difficulty breathing while lying flat (orthopnea)

- Episodes of waking up from sleep gasping for air (paroxysmal nocturnal dyspnea)

- Acute pulmonary edema

Other cardiac symptoms of heart failure include chest pain/pressure and palpitations. Common noncardiac signs and symptoms of heart failure include loss of appetite, nausea, weight loss, bloating, fatigue, weakness, low urine output, waking up at night to urinate, and cerebral symptoms of varying severity, ranging from anxiety to memory impairment and confusion.

Symptoms usually include one or more of the following: orthopnea (difficulty breathing while lying flat), dyspnea (shortness of breath on exertion), pitting edema (swelling), cough, frequent night-time urination, excessive weight gain during the last month of pregnancy (1-2+ kg/week; two to four or more pounds per week), palpitations (sensation of racing heart-rate, skipping beats, long pauses between beats, or fluttering), and chest pain.

The shortness of breath is often described by PPCM patients as the inability to take a deep or full breath or to get enough air into the lungs. Also, patients often describe the need to prop themselves up overnight by using two or more pillows in order to breathe better. These symptoms, swelling, and/or cough may be indications of pulmonary edema (fluid in the lungs) resulting from acute heart failure and PPCM.

Unfortunately, patients and clinicians sometimes dismiss early symptoms because they appear to be typical of normal pregnancy. Yet, early detection and treatment are critically important to the patient with PPCM. Delays in diagnosis and treatment of PPCM are associated with increased morbidity and mortality.

It is important to note that occasionally patients present with other signs or symptoms. This is demonstrated by one report of a woman with liver failure five weeks postpartum who was being considered for liver transplant. An echocardiogram was performed and revealed PPCM and heart failure as the cause of her severe liver failure. Conventional heart failure medications were administered. She survived and completely recovered from both the liver failure and PPCM.

It is also quite common for women to present with evidence of having an embolus (clot) passing from the heart to a vital organ, causing such complications as stroke, loss of circulation to a limb, even coronary artery occlusion (blockage) with typical myocardial infarction (heart attack).

For these reasons, it is paramount that clinicians hold a high suspicion of PPCM in any peri- or postpartum patient where unusual or unexplained symptoms or presentations occur.

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

The signs and symptoms associated with myocarditis are varied, and relate either to the actual inflammation of the myocardium or to the weakness of the heart muscle that is secondary to the inflammation. Signs and symptoms of myocarditis include the following:

- Chest pain (often described as "stabbing" in character)

- Congestive heart failure (leading to swelling, shortness of breath and liver congestion)

- Palpitations (due to abnormal heart rhythms)

- Sudden death (in young adults, myocarditis causes up to 20% of all cases of sudden death)

- Fever (especially when infectious, e.g. in rheumatic fever)

- Symptoms in young children tend to be more nonspecific, with generalized malaise, poor appetite, abdominal pain, and chronic cough. Later stages of the illness will present with respiratory symptoms with increased work of breathing, and is often mistaken for asthma.

Since myocarditis is often due to a viral illness, many patients give a history of symptoms consistent with a recent viral infection, including fever, rash, diarrhea, joint pains, and easily becoming tired.

Myocarditis is often associated with pericarditis, and many people with myocarditis present with signs and symptoms that suggest myocarditis and pericarditis at the same time.

The clinical course of HCM is variable. Many people with HCM are asymptomatic or mildly symptomatic, and many of those carrying disease genes for HCM do not have clinically detectable disease. The symptoms and signs of HCM include shortness of breath due to stiffening and decreased blood filling of the ventricles, exertional chest pain (sometimes known as angina) due to reduced blood flow to the coronary arteries, uncomfortable awareness of the heart beat (palpitations), as well as disruption of the electrical system running through the abnormal heart muscle, lightheadedness, weakness, fainting and sudden cardiac death.

Dyspnea is largely due to increased stiffness of the left ventricle (LV), which impairs filling of the ventricles, but also leads to elevated pressure in the left ventricle and left atrium, causing back pressure and interstitial congestion in the lungs. Symptoms are not closely related to the presence or severity of an outflow tract gradient. Often, symptoms mimic those of congestive heart failure (esp. activity intolerance and dyspnea), but treatment of each is different. Beta blockers are used in both cases, but treatment with diuretics, a mainstay of CHF treatment, will exacerbate symptoms in hypertrophic obstructive cardiomyopathy by decreasing ventricular preload volume and thereby increasing outflow resistance (less blood to push aside the thickened obstructing tissue).

Major risk factors for sudden death in individuals with HCM include prior history of cardiac arrest or ventricular fibrillation, spontaneous sustained ventricular tachycardia, family history of premature sudden death, unexplained syncope, LV thickness greater than or equal to 30 mm, abnormal exercise blood pressure and nonsustained ventricular tachycardia.

High-output heart failure is a heart condition that occurs when the cardiac output is higher than normal due to increased peripheral demand. There is a circulatory overload which may lead to pulmonary edema secondary to an elevated diastolic pressure in the left ventricle. These individuals usually have a normal systolic function but symptoms are those of heart failure. With time, this overload causes systolic failure. Ultimately cardiac output can be reduced to very low levels.

It may occur in situations with an increased blood volume, from excess of water and salt (kidney pathology, excess of fluid or blood administration, treatment with retaining water steroids), chronic and severe anemia, large arteriovenous fistula or multiple small arteriovenous shunts as in HHT or Paget's disease of bone, some forms of severe liver or kidney disorders, hyperthyroidism, and wet beriberi, and acutely in septic shock, especially caused by Gram-negative bacteria.

Signs and symptoms of ischemic cardiomyopathy include sudden fatigue, shortness of breath, dizziness and palpitations.

Heart failure with preserved ejection fraction (HFpEF) is a form of congestive heart failure where in the amount of blood pumped from the heart's left ventricle with each beat (ejection fraction) is greater than 50%. Approximately half of people with heart failure have HFpEF, while the remainder display a reduction in ejection fraction, or heart failure with reduced ejection fraction (HFrEF).

HFpEF is characterized by abnormal diastolic function, which manifests as an increase in the stiffness of the heart's left ventricle and a decrease in left ventricular relaxation when filling with blood before the next beat. There is an increased risk for atrial fibrillation and pulmonary hypertension. Risk factors for HFpEF include hypertension, hyperlipidemia, diabetes, smoking, and obstructive sleep apnea. There is a query about the relationship between diastolic heart failure and HFpEF.

Dilated cardiomyopathy (DCM) is a condition in which the heart becomes enlarged and cannot pump blood effectively. Symptoms vary from none to feeling tired, leg swelling, and shortness of breath. It may also result in chest pain or fainting. Complications can include heart failure, heart valve disease, or an irregular heartbeat.

Causes include genetics, alcohol, cocaine, certain toxins, complications of pregnancy, and certain infections. Coronary artery disease and high blood pressure may play a role, but are not the primary cause. In many cases the cause remains unclear. It is a type of cardiomyopathy, a group of diseases that primarily affects the heart muscle. The diagnosis may be supported by an electrocardiogram, chest X-ray, or echocardiogram.

In those with heart failure treatment may include medications in the ACE inhibitor, beta blocker, and diuretic families. A low salt diet may also be helpful. In those with certain types of irregular heartbeat, blood thinners or an implantable cardioverter defibrillator may be recommended. If other measures are not effective a heart transplant may be an option in some.

About 1 per 2,500 people are affected. It occurs more frequently in men than women. Onset is most often in middle age. Five-year survival rate is about 50%. It can also occur in children and is the most common type of cardiomyopathy in this age group.

People with TIC most often present with symptoms of congestive heart failure and/or symptoms related to their irregular heart rhythm. Symptoms of congestive heart failure can include shortness of breath, ankle swelling, fatigue, and weight gain. Symptoms of an irregular heart rhythm can include palpitations and chest discomfort.

The timecourse of TIC is most well-studied in experiments on animals. Researchers have found that animals began to exhibit abnormal changes in blood flow after just one day of an artificially generated fast heart rate (designed to simulate a tachyarrythmia). As their TIC progresses, these animals will have worsening heart function (e.g.: reduced cardiac output and reduced ejection fraction) for 3–5 weeks. The worsened heart function then persists at a stable state until the heart rate is returned to normal. With normal heart rates, these animals begin to demonstrate improving heart function at 1–2 days, and even complete recovery of ejection fraction at 1 month.

Human studies of the timecourse of TIC are not as robust as animal studies, though current studies suggest that the majority of people with TIC will recover a significant degree of heart function over months to years.

The typical presentation of takotsubo cardiomyopathy is a sudden onset of chest pain associated with ECG changes mimicking a myocardial infarction of the anterior wall. During the course of evaluation of the patient, a bulging out of the left ventricular apex with a hypercontractile base of the left ventricle is often noted. It is the hallmark bulging out of the apex of the heart with preserved function of the base that earned the syndrome its name "tako tsubo", or octopus pot in Japan, where it was first described.

Stress is the main factor in takotsubo cardiomyopathy, with more than 85% of cases set in motion by either a physically or emotionally stressful event that prefaces the start of symptoms. Examples of emotional stressors include grief from the death of a loved one, fear of public speaking, arguing with a spouse, relationship disagreements, betrayal, and financial problems. Acute asthma, surgery, chemotherapy, and stroke are examples of physical stressors. In a few cases, the stress may be a happy event, such as a wedding, winning a jackpot, a sporting triumph, or a birthday.

Takotsubo cardiomyopathy is more commonly seen in postmenopausal women. Often there is a history of a recent severe (usually negative, sometimes happy) emotional or physical stress.

Tachycardia-induced cardiomyopathy (TIC) is a disease where prolonged tachycardia (a fast heart rate) or arrhythmia (an irregular heart rhythm) cause an impairment of the myocardium (heart muscle), which can result in heart failure. People with TIC may have symptoms associated with heart failure (e.g. shortness of breath or ankle swelling) and/or symptoms related to the tachycardia or arrhythmia (e.g. palpitations). Though atrial fibrillation is the most common cause of TIC, several tachycardias and arrhythmias have been associated with the disease.

There are no formal diagnostic criteria for TIC. Thus, TIC is typically diagnosed when (1) tests have excluded other causes of cardiomyopathy and (2) there is improvement in myocardial function after treatment of the tachycardia or arrhythmia. Treatment of TIC can involve treating the heart failure as well as the tachycardia or arrhythmia. TIC has a good prognosis with treatment, with most people recovering some to all of their heart function.

The number of cases that occur is unclear. TIC has been reported in all age groups.

Myocarditis, also known as inflammatory cardiomyopathy, is inflammation of the heart muscle. Symptoms can include shortness of breath, chest pain, decreased ability to exercise, and an irregular heartbeat. The duration of problems can vary from hours to months. Complications may include heart failure due to dilated cardiomyopathy or cardiac arrest.

Myocarditis is most often due to a viral infection. Other causes include bacterial infections, certain medications, toxins, and autoimmune disorders. A diagnosis may be supported by an electrocardiogram (ECG), increased troponin, heart MRI, and occasionally a heart biopsy. An ultrasound of the heart is important to rule out other potential causes such as heart valve problems.

Treatment depends on both the severity and the cause. Medications such as ACE inhibitors, beta blockers, and diuretics are often used. A period of no exercise is typically recommended during recovery. Corticosteroids or intravenous immunoglobulin (IVIG) may be useful in certain cases. In severe cases an implantable cardiac defibrillator or heart transplant may be recommended.

In 2013, about 1.5 million cases of acute myocarditis occurred. While people of all ages are affected, the young are most often affected. It is slightly more common in males than females. Most cases are mild. In 2015 cardiomyopathy, including myocarditis, resulted in 354,000 deaths up from 294,000 in 1990. The initial descriptions of the condition are from the mid-1800s.

Clinical manifestations of HFpEF are similar to those observed in HFrEF and include shortness of breath including exercise induced dyspnea, paroxysmal nocturnal dyspnea and orthopnea, exercise intolerance, fatigue, elevated jugular venous pressure, and edema.

Patients with HFpEF poorly tolerate stress, particularly hemodynamic alterations of ventricular loading or increased diastolic pressures. Often there is a more dramatic elevation in systolic blood pressure in HFpEF than is typical of HFrEF.