The left ventricle is an integral part of the cardiovascular system. Left ventricular contraction forces oxygenated blood through the aortic valve to be distributed to the entire body. With such an important role, decreased function caused by injury or maladaptive change can induce symptoms of the disease.
Issues of Concern
Heart failure (HF) often results from poor left ventricular function. Reduced diastolic filling and ejection fraction can both lead to less blood leaving the heart into systemic circulation. HF correlates with structural changes in the ventricular wall such as ventricular dilation and mural thinning. Alterations in various components of the myocardium precede these ventricular changes such as focal myocyte loss and fibrotic replacement, as well as hypertrophic myocyte activity leading to a thicker ventricular wall. These myocardial changes lead to a decrease in the ability of the individual myocytes to contract with sufficient speed and force to maintain cardiac output necessary to meet bodily needs. 
Cardiac muscle tissue is only found in the heart. Each myocyte contains a single nucleus and many mitochondria for high energy output. Cardiac muscle is involuntary, striated, and possesses an extensive capillary network. Cardiomyocytes are the individual muscle cells that are organized into sarcomeres and interconnected via intercalated discs. The interconnections allow synchronized contraction of the cardiac myofibrils. Each contraction is initiated by the release of calcium into the cytosol. T-tubules facilitate the conversion of electrical impulses from Purkinje fibers into mechanical contraction, called excitation-contraction coupling, by activating L-type calcium channels to allow calcium into the cytosol. This calcium binds to ryanodine receptors in the sarcoplasmic reticulum which induces ventricular contraction.  The amount of calcium transiently determines the contractility of the heart. Physiological or pathological increases in cardiac demand, such as greater afterload, induces adaptive changes in the left ventricle including myocyte hypertrophy, or fibroblast proliferation leading to fibrosis, vascularization, and even cell death. 
From conception, the cells from the primary cardiac crescent form bilaterally within the embryonic disc and migrate to the cervical region to form the primary heart tube. Subsequent divisions and contributions from the bulbus cordis develop into the right ventricle while the primitive ventricle of the primary cardiac crescent forms the left ventricle. During subsequent weeks, the primitive heart folds into an "s" shape, which places the chambers and major vessels into alignment and shape that mirrors an adult heart. The partitioning of the atria and ventricles by the interatrial, interventricular, and atrioventricular septum proceed, followed by the formation of the semilunar valves. 
Congenital defects of the left ventricle include hypoplastic left heart syndrome. This condition is characterized by an underdeveloped left ventricle secondary to a small, poorly formed mitral valve, aortic valve, and/or ascending aorta. The number of affected structures coincides with the severity of this defect. The underdeveloped left ventricle is unable to adequately pump blood to the body, so the newborn will undergo surgery to bypass the poorly functioning left side of the heart, and make the right ventricle the main pump to the body.  Most affected newborns also have an atrial septal defect, so medication is given to help the foramen ovale remain patent as well as help lower their blood pressure and remove excess fluid.
Organ Systems Involved
The left ventricle connects nearly all organ systems through its function to pump oxygenated blood to the body. Left ventricular failure would likely result in impairment to all other organ systems. Organs may react to low ventricular function by initiating mechanisms to increase blood delivery. A person might experience syncopal episodes due to a lack of blood flow to the brain, or their kidneys might start to release renin to elevate blood pressure. Decreased cardiac output can also lead to adrenal release of epinephrine to increase heart rate, and subsequently blood pressure, thus increasing blood supply to vital organs such as the brain. Left ventricular failure may cause blood to back up into the lungs and cause pulmonary edema. This edema can lead to pulmonary hypertension and excessive strain to the right atrium and ventricle. The fluid will again back up, this time into the vena cava, and can cause liver pathologies and cause portal hypertension.
Providing sufficient cardiac output to maintain blood flow to other organ systems is the primary function of the left ventricle. Cardiac output is the result of systolic contraction of the left ventricle, which can be influenced by preload, afterload, and contractility.
Cardiac output (CO) is defined as the amount of blood that is pumped out of the heart in a given time. Heart rate (HR) is the number of heartbeats in a given time, often recorded as beats per minute (bpm). Stroke volume (SV) is the volume of blood ejected in a single ventricular contraction. Cardiac output can be calculated using the following equations:
- CO = HR * SV
- SV = end-diastolic volume (EDV) – end-systolic volume (ESV)
Cardiac output cannot be measured clinically, so ejection fraction is a commonly used index to estimate heart contractility. Left ventricular ejection fraction (LVEF) is the volume of blood pumped out of the heart during systole relative to the volume in the left ventricle at the end of diastole. LVEF is calculated using the following equation:
Factors Affecting Cardiac Output
Preload is the load on ventricular muscle during diastole. The load is caused by the volume of blood that fills the ventricle as it rests between contractions. Higher preload volumes generally increase contractility through the Frank-Starling mechanism. This mechanism occurs when the preload volume lengthens the myocyte sarcomere length closer to the optimal overlap of actin and myosin.
Afterload is the pressure that the left ventricle must push against during each contraction. Conditions like hypertension, atherosclerosis, and aortic stenosis all require the left ventricle to work harder to overcome the elevated afterload pressure. If this occurs chronically, the left ventricle will undergo hypertrophic adaptations which can lead to pathology.
Contractility is the inotropic state of the heart muscle. The intracellular calcium levels greatly influence heart contractility with higher levels inducing a stronger contraction. Medications like digoxin are given to increase heart contractility via myocyte contractile performance and electrophysiological variables do so by raising intracellular calcium levels. These medications are therapeutic for those who suffer from chronic left ventricular dysfunction. Therapy can normalize action potential characteristics and result in improved left ventricular pump function in the setting of left ventricular failure. 
Evaluation of left ventricular function is the result of three indices: end-diastolic left ventricular chamber size, LVEF, and mean velocity of circumferential fiber shortening (MVCFc), which reflects heart muscle performance. All of these indices of measurements are preload and afterload-dependent and, therefore, can influence contractility, or relative inotropic sensitivity. 
The left ventricle pumps blood at higher pressures compared to the rest of the other heart chambers, as it faces a much higher workload and mechanical afterload. In comparison to that of the right ventricle, the free wall of the left ventricle is much thicker.
The electrophysiology of the left ventricle starts at the sinoatrial (SA) node which initiates an action potential. This action potential is carried across the atria, causing contraction, to the atrioventricular (AV) node. The AV node delays the electrical current by about 100ms before transmitting the impulse to the atrioventricular bundle of His. The electrical impulse then travels down the right and left bundle branches to the Purkinje fibers. When the action potential reaches the ventricular contractile fibers, excitation-contraction coupling induces calcium influx causing synchronized contraction starting at the heart apex and progressing upwards. 
Heart disease can manifest in different ways such as electrocardiogram (ECG) abnormalities, palpitations, wall motion abnormalities, or a change in chamber geometry. For example, heart failure is a clinical diagnosis that can be the result of a multitude of different structural and functional cardiac disorders that affect intrinsic myocardial contractility. It is largely a clinical diagnosis and is characterized by the inability of the ventricle to fill with blood or eject blood properly. A patient might exhibit systolic as well as diastolic dysfunction, and present with dyspnea, fatigue, and fluid retention. ECGs may be used to assess heart electrical activity and can unearth findings that may be resulting in heart failure like ventricular tachycardia, ventricular fibrillation, left ventricular hypertrophy, and myocardial infarctions. Stress testing and echocardiograms are noninvasive diagnostic exam methods used to assess for cardiac lesions and monitor myocardial functionality and may reveal chamber size abnormalities, wall motion abnormalities, or improper valve function. It has been shown that stress echocardiography in combination with various stressors can detect significant coronary stenosis with accuracy ranging from 80 to 90%, making it a powerful prognostic tool in those with chronic coronary artery disease. 
Important to the diagnosis of heart failure is left ventricular ejection fraction (LVEF), which is evaluated with an echocardiogram. It is a load-dependent test and indicator of left ventricular performance. The fraction percentage identifies the different categories of heart failure: preserved ejection fraction greater than or equal to 50%, mid-range left ventricular ejection fraction 41-49%, and reduced ejection fraction less than or equal to 40%.  This differentiation between the preserved, midrange, and reduced LVEF is important for continued quality of care performance and measurement in heart failure patients.
The circumferential fiber shortening (MCVFc) is another measurement that can aid in determining ventricular performance as a direct relation to muscle function. It is an index of myocardial performance relative to wall stress. There is an inverse linear relationship between end-systolic wall stress and the velocity of circumferential fiber shortening, the index of which is a sensitive measure of the cardiac contractile state independent of preload and accounting for afterload. 
Tissue Doppler is another noninvasive method of testing the systolic and diastolic function and performance of the left ventricle. It is used to assess for changes in the myocardium due to strain, twists, rotations that are distinct from previous tests.
Left ventricular heart failure can result from a variety of pathologies such as ischemia, excessive peripheral demands, high output failure, volume overload, pressure, and volume overload, and primary muscle disease. Four determinants of left ventricular performance are an intrinsic decrease in muscle contractility, an increase in systemic afterload causing decreased cardiac output, increased preload that pushes fluid into the lungs causing pulmonary congestion, and increased heart rate associated with sympathetic tone. 
Left ventricular hypertrophy can occur when the heart contracts against a high pressure chronically. The high pressure can be attributed to conditions like hypertension or aortic stenosis. Over time, the heart adapts to this stress through myocyte hypertrophy. However, this process is a pathologic mechanism as the ventricular wall thickens, which decreases overall left ventricular function. On the contrary, non-pathologic hypertrophy can result from exercise where the myocytes increase in size but do not cause wall thickening associated with decreased ventricular function.
Per the CDC, 1 in 4 people with heart disease die each year in the United States, making it the leading cause of death in both men and women. Heart failure is still a challenge to many health care providers and is associated with higher rates of readmissions and increased morbidity and mortality. Treatment methods will vary based on the nature and extent of the pathophysiology. The primary goals of management are to improve prognosis and reduce morbidity and mortality with appropriate therapies.  If the patient is admitted to the hospital, an additional goal would be to reduce rates of readmission as well as the length of stay. Additionally, addressing and managing other comorbidities that could enhance cardiac dysfunction is of great importance for positive outcomes.