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StatPearls . Endowment Island (FL): StatPearls Publishing; 2021 Jan-.



The heart muscles line the myocardium, or center layer that the love walls, and also are responsible because that the contractile duty of the cardiac pump. Created of cardiomyocytes, the love muscle has actually distinctive cellular and also physiological features permitting it to generate pressure to maintain adequate tissue and also organ perfusion transparent the entire body. Love muscle renders up among the more quickly functioning embryonic offal that proceeds to contract and beat from breakthrough throughout a lifetime. Supplied by a facility system that coronary vasculature, cardiac lymphatics, and also autonomic innervation, cardiomyocytes line the thickest great of every chamber of the heart. Cardiovascular conditions are the leading reason of mortality worldwide. A vast variety of these illness involve the love muscles with diverse mechanisms the pathophysiology, resulting in contractile dysfunction, cell damage and also death, and also cardiac pump failure. However, plenty of interventions, therapy options, and also therapies space aimed in ~ minimizing damage, restoring functionality, avoiding the occurrence, and also reducing the risk of cardiovascular disease.

Structure and Function

Three distinct layers make up the love walls, from inner to outer:


The muscles of the heart, termed the myocardium, consist of the middle and thickest class of the love wall. This great lies between the single-cell endocardium layer, i m sorry lines the inside chambers, and also the outer epicardium, which makes up part of the pericardium the surrounds and protects the heart. Histologically, heart muscles are composed the cells referred to as cardiomyocytes the have unique structures and properties correlating to their contractile function.<1> Cardiomyocytes space striated, uninucleate muscle cells discovered exclusively in the heart muscle. A distinct cellular and physiological function of cardiomyocytes space intercalated discs, i beg your pardon contain cell adhesions together as gap junctions, come facilitate cell-cell communication. These discs reduce inner resistance and allow activity potentials come spread quickly throughout the whole heart muscle via the i of fee ions. Thus, the heart muscle acts as a sensible syncytium with fast synchronized contractions that room responsible for pumping blood throughout the body. Functionally, the heart muscles depend on electrochemical gradients and the potentials to create contractile force for each heartbeat.

The sinus node, situated within the appropriate atrial myocardium, spontaneously depolarizes and thus determines the heart rate. This depolarizations are currents of ion influx the are carried from the sinus node come the love muscle via conducting cells. Once the depolarization reaches the heart muscle, voltage-gated sodium channels open, permitting a rapid influx of salt ions into the cardiomyocytes, depolarizing the cells. The positive membrane potential root cause voltage-gated potassium and also then calcium channels to open, enabling potassium to sirloin out and calcium to sirloin in. The initial influx of calcium is vital for the second release that calcium indigenous the sarcoplasmic reticulum found within the heart muscle cells. The build-up of intracellular calcium ion binds come troponin C, relocating tropomyosin beside to enable actin-myosin binding and cross-bridge to ride bicycle responsible for muscle contraction.<1> The amount of calcium exit is straight proportional come the lot of actin-myosin interaction allowed and therefore correlates with the contractile force of the love muscle generated. Physiologically, this corresponds with parameters such as stroke volume, ejection fraction, and also cardiac output supplied to assess heart function. In ~ the finish of every cycle, calcium gets revitalized to the sarcoplasmic illusion via SERCA (Sarco(endo)plasmic reticulum (SER) Ca2+ ATPase) pumps when sodium-potassium and also sodium-calcium ATPase pumps restore the cardiomyocyte membrane potential for this reason the cycle have the right to repeat v the following incoming depolarization.<1>


The love muscle originates native the mesoderm layer and begins forming throughout the 3rd week of embryonic development. The mesoderm serves as the primary source for myocardial precursor cells, which comprise the cardiogenic or primary heart field during early development. A primitive, horseshoe-shaped endothelial heart tube is formed and begins contracting come facilitate the embryo’s early circulation system. Within the following several weeks, the proliferation of cardiomyocytes is crucial for broadening the myocardial layer and generating the multichambered mechanism of the mature heart.<2> when existing cardiomyocytes add to the development of the myocardium via proliferation and organization, brand-new heart muscle cells are additionally recruited from adjacent mesenchymal layers the further increases the muscle layer.<2> complying with myocardial development, the heart walls undergo more maturation, compaction, and trabeculation. Dilatations or swellings of the heart pipe embryonic structures along with neural crest cell migration facilitate the breakthrough of the chambers and also inflow/outflow tracts. These processes an outcome in a mature and completely functional, contracting heart by the eighth embryonic week and throughout adulthood.

Blood Supply and also Lymphatics

The love muscles’ blood supply comes directly from the device of coronary arteries the runs in ~ the epicardial layer. Two key coronary arteries, the left coronary artery (LCA) and also the ideal coronary artery (RCA), branch straight off the aorta via the coronary Ostia. These arteries and also their branches supply tributary arteries that operation perpendicular come the love surface and also transverse from the epicardium, v the myocardium, and also down to the endocardium.<3> The LCA easily branches into the left anterior diminish (LAD) coronary artery and also the left circumflex (LCX) coronary artery. The LAD runs vertically under the interventricular groove towards the apex and supplies blood come the anterior left ventricular myocardium, the anterior two-thirds of the interventricular septal myocardium, and the anterolateral papillary muscle connecting the mitral valves. The LCX courses horizontally along the atrioventricular groove and gives increase to the left obtuse marginal coronary artery, together providing the lateral and posterior left ventricular myocardium. The RCA runs horizontally follow me the appropriate atrioventricular groove and gives increase to the appropriate acute marginal coronary artery, which provides the right ventricular myocardium. The RCA likewise gives increase to the posterior diminish artery (PDA) in about 90% of the human population (the PDA comes from the LCX in the other roughly 10%), which provides the posterior myocardium that both ventricles, the posterior one-third of the interventricular septal myocardium, and also the posteromedial papillary muscle that the mitral valves.<3> Blood flow via the coronary arteries come the myocardium occurs throughout diastole and ventricular relaxation via the passive flow of blood into the aortic Ostia. Throughout systole and also ventricular contraction, the coronary arteries come to be compressed, and thus impedes myocardial blood flow.

The venous mechanism of the heart muscles runs parallel to the coronary arteries. Venous drainage the the left ventricular myocardium is completed by the interventricular vein and also the great cardiac vein, which drains right into the coronary sinus, found in the posterior right atrioventricular groove, which then drains right into the right atrium.<3> The anterior cardiac veins are responsible for draining blood indigenous the ideal ventricular myocardium directly into the ideal atrium.<3>

The cardiac lymphatic drainage device is consisted of of lymphatic capillaries and pre-collector vessels organized in plexuses within every of the heart wall layers.<4> this lymphatic vessels and also plexuses circulation from subendocardium, v the myocardium, up through the subepicardium, right into the mediastinal lymph nodes, and also ultimately draining into both left and right venous angles between the interior jugular veins and the subclavian veins. The source of flow for lymphatic drainage originates from contractions that the myocardium, which generate pressure to propel fluid movement with the device to the lymph nodes.


Heart muscles are innervated generally by 2 nerves, the accelerans nerve and also the vagus nerve, which provide sympathetic and parasympathetic stimulation from the autonomic concerned system, respectively. Intrinsic ganglia for the myocardium are existing in the epicardium, i beg your pardon receives signal from post-ganglionic sympathetic relations coming from the accelerans nerve and also pre-ganglionic parasympathetic connections from the vagus nerve.<5> most post-ganglionic sympathetic relations synapse directly with the heart muscle cells, releasing norepinephrine as the major neurotransmitter.<5> upon binding, norepinephrine stimulates beta-adrenergic receptor to rise contractility of the myocardium via enhancing calcium influx. Preganglionic parasympathetic fibers synapse very first with the epicardial intrinsic ganglia and also then post-ganglionic neurons directly synapse with the myocardium.<5> Acetylcholine is the main neurotransmitter for myocardial parasympathetic signals, exhilaration on muscarinic (M2) receptor on the cardiomyocytes.


The muscle great of the love is termed the myocardium and also is consisted of of cardiomyocytes. The myocardium is discovered in the wall surfaces of all 4 chambers the the heart, though it is more thick in the ventricles and thinner in the atria. This disparity is because of the difference in the generation of the pressure of contraction required for propelling blood between the atria and the ventricles, v ventricles inquiry much an ext power.

Physiologic Variants

Chronic primary hypertension is a common and prevalent disease affecting a huge percentage of the United claims population. Over lengthy periods, chronic systemic hypertension can an outcome in structural and also functional alters to the love muscle wall. Because of chronic boosts in afterload, the press in i beg your pardon the left ventricular muscle need to contract against increased average arterial pressure, the love muscle responds with compensatory cardiomyocyte hypertrophy. The ventricular muscle wall thickens come reduce wall surface stress through a resulting increase in the wall thickness come the chamber diameter ratio.<6> Left ventricular hypertrophy (LVH) for this reason characteristically demonstrates a geometry that concentric thickness and also is a physiological response to and also a typical complication of also mild chronic hypertension.<6> physical examination findings of LVH may encompass an enlarged allude of maximal advertise (PMI) and an S4 gallop upon cardiac apex auscultation.

Normal aging processes change heart muscle structurally and also physiologically. Arteries end up being less compliant and stiffen end time, and in older years, this results in boost in afterload because of greater pressure against which the love muscle need to contract. Together a compensatory response, left ventricular thickness increases from cardiomyocyte hypertrophy. Over time, cardiomyocytes diminish with period from apoptosis, necrosis, or autophagy resulting in an as whole decrease in cardiomyocyte number in age heart muscle.<7> together a compensatory mechanism, the staying cardiomyocytes may hypertrophy or experience pathological remodeling. These changes an outcome in a diminish in cardiac compliance and rise in wall surface stiffness. In ~ the love muscle cells, age-related transforms induce a transition from alpha-myosin hefty chain come the beta-myosin heavy chain with diminished cross-bridge to ride bicycle activity.<7> This condition ultimately leads to contractile decrease and diastolic dysfunction in the aging heart muscle. Calcium homeostasis is also impacted during aging processes due to a reduced capability of SERCA pumps and also the sodium-calcium pumps to effectively restore relaxing membrane potential calcium levels.<7> Disrupted calcium homeostasis affects heart muscle be sure mechanics and thus leads to diastolic dysfunction.

Surgical Considerations

A significant, however underrecognized, heart muscle complication after non-cardiac surgical procedure is perioperative myocardial injury (PMI), i beg your pardon is distinct from myocardial infarction. Risk factors for PMI before and after surgery incorporate age better than or equal to 65 years and also a preexisting background of atherosclerotic disease. PMI is an acute rise in high-sensitivity cardiac troponin T (hs-cTn) plasma concentrations.<8> PMI often presents without chest pain, dyspnea, or other typical cardiac injury symptoms and also is thus routinely missed throughout clinical workups perioperatively. However, PMI correlates v a significantly increased risk of 30-day mortality post-noncardiac surgery.<8> To efficiently diagnose PMI, hs-cTn screening should be supplied perioperatively come detect and also quantify cardiomyocyte injury to minimize the danger of short and long-term mortality.

Clinical Significance

Coronary artery an illness (CAD), additionally termed ischemic love disease, is the most prevalent cardiovascular condition and the leading reason of global mortality, with far-reaching implications and results for heart muscle functionality. CAD is defined by the development of atherosclerotic plaques in ~ the coronary arteries resulting in a diminish in blood flow and oxygen and nutrient shipment to the myocardium. Manifestations the CAD space termed acute coronary syndromes (ACS) and also include steady angina, turbulent angina, and others native the supply-demand mismatch of poor oxygen perfusion indigenous at the very least 70% occlusion of the myocardial vascular supply. The most severe manifestations that CAD space myocardial infarctions, colloquially termed “heart attacks.” Myocardial infarctions (MIs) divide into ST-segment elevation myocardial infarctions (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI), escape on complete or near-total coronary vascular occlusions, respectively, and subsequent findings on electrocardiogram (EKG).

The ar of myocardial infarctions within the heart deserve to be generally localized via which certain leads are impacted with abnormal ST-segment and/or T-wave morphologies on one EKG. MIs demonstrate cardiomyocyte necrosis, and also diagnostic findings incorporate positive cardiac troponin (cTn) tests and creatinine kinase myocardial band (CK-MB) tests.<9> following MIs, the affected heart muscle wall surface is regularly weaker 보다 it was prior to the MI from cell injury and also death, inflammation, and also fibrotic replacement that decreases love muscle contractile function, which boosts the hazard for love failure, totally free wall ruptures, arrhythmias, suddenly cardiac death, and also other complications. Therapy for MIs contains pharmacotherapy such as antiplatelet drugs and fibrinolysis, interventions such together percutaneous coronary interventions (PCIs), or surgeries such together coronary artery bypass grafting (CABG) aimed in ~ restoring perfusion and vascularization the the myocardium.<9>

Cardiomyopathies space inherited or acquired illness of the love muscle that impact structure and also functionality in the lack of various other cardiovascular condition processes, such together CAD. Hypertrophic cardiomyopathy (HCM) is the most usual genetically inherited heart condition and follows an autosomal dominant inheritance pattern. The pathophysiology of HCM originates from mutations in myocardial sarcomere genes bring about myofibrillar disarray, serious thickening, hypertrophy that the heart muscle wall, and diastolic dysfunction. Manifestations that HCM incorporate dyspnea, syncope, palpitations, and sudden death, and most typically presents in adolescence. Dilated cardiomyopathy (DCM) is defined by eccentric hypertrophy, dilation the the cardiac muscle wall, and also systolic dysfunction.<10> DCM is the final myocardial response to a selection of genetic and also environmental stresses such as chronic alcohol abuse, viral or helminth infections, certain chemotherapies, and other etiologies with the most usual being idiopathic DCM.<11> treatment for cardiomyopathies contains pharmacotherapy to reduce heart muscle demand such as calcium-channel blockers or beta-blockers, implantable cardioverter-defibrillator (ICD) placements to protect against life-threatening arrhythmias or heart transplantation.

Myocarditis is the term because that inflammation of the heart muscle and has number of etiologies. The most common etiology in the Western civilization is famous infections (infectious myocarditis), but other causes include toxicity reactions or allergy to drugs, autoimmune diseases, or various other infections (bacterial, fungal, parasitic). Myocarditis entails damage and loss of both cardiomyocytes and cardiac vascular endothelial cells, both of i m sorry are common targets of infection from inflammatory processes and also white blood cell (often lymphocytic) infiltration right into the heart muscle wall.<12> Complications encompass interstitial cardiac fibrosis, wall motion abnormalities, arrhythmias, love failure, myocardial infarctions, reduced ejection fraction, and sudden cardiac death.<12> Myocarditis has actually a diverse presentation v non-specific symptoms such as chest pain, dyspnea, flu-like manifestations, however can likewise be symptomless.

Heart fail (HF) is the typical end-stage pathway and clinical manifestation that cardiac pump dysfunction native a variety of etiologies, including plenty of diseases influence the love muscle. HF can be categorized into different groups such as acute vs. Chronic, right heart vs. Left heart, systolic (reduced ejection fraction) vs. Diastolic (preserved ejection fraction), each presenting with unique clinical characteristics. HF is essentially identified as the inability of the heart to pump adequately resulting in congestion, reduced organ perfusion, and functional impairment.<1> Etiologies and also risk determinants for HF are diverse and encompass processes such as myocardial injury or infarction, CAD, chronic hypertension, valvular dysfunction, arrhythmias, cardiomyopathies, and numerous other pathways. The pathophysiology leading to HF involves complex interactions of equipment such together neurohormonal activation, peripheral vascular effects, and also physiological procedures within the love muscle itself.

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<1> treatment for HF involves pharmacotherapy such together ACE inhibitors and beta-blockers come decrease heart stress and also workload or inotropes to increase contractility. Therapies for advanced heart failure incorporate mechanical circulatory assistance such together ventricular assist gadgets (VADs) or heart transplantation.