Lusitropy

Lusitropy is the rate of myocardial relaxation. The increase in cytosolic calcium of cardiomyocytes via increased uptake leads to increased myocardial contractility (positive inotropic effect), but the myocardial relaxation, or lusitropy, decreases. This should not be confused, however, with catecholamine-induced calcium uptake into the sarcoplasmic reticulum, which increases lusitropy.

Positive

Increased catecholamine levels promote positive lusitropy, enabling the heart to relax more rapidly. This effect is mediated by the phosphorylation of phospholamban and troponin I via a cAMP-dependent pathway. Catecholamine-induced calcium influx into the sarcoplasmic reticulum increases both inotropy and lusitropy. In other words, a quicker reduction in cytosolic calcium levels (because the calcium enters the sarcoplasmic reticulum) causes an increased rate of relaxation (+ lusitropy), however that also enables a greater degree of calcium efflux, back into the cytosol, when the next action potential arrives, thereby increasing inotropy as well. Do not confuse this calcium mechanism with calcium uptake from the extracellular fluid. Increased calcium uptake from the extracellular fluid into the cytoplasm decreases lusitropy in the absence of catecholamine stimulation, but increased calcium uptake into the sarcoplasmic reticulum, via catecholamines, increases lusitropy and inotropy.

Negative

Relaxation of the heart is negatively impacted by the following factors:

1) Calcium overload - too much intracellular calcium
2) Reduced rate of calcium removal from myocyte through pumps - if calcium is not removed from the cell quickly enough.

a) Plasma membrane Calcium ATPase (Ca ATPase) - this primary active transporter pumps calcium out of the myocyte between beats

b) Sodium-Calcium (Na/Ca) exchanger - this secondary active transporter pumps calcium out of cell between beats

3) Impaired Sarco-Endoplasmic Reticulum Calcium ATPase (SERCA) - this primary active transporter pumps calcium from the cytoplasm of the myocyte into its sarco-endoplasmic reticulum.

Therefore, any impairment of the transporters in (2) and (3) would have a negative lusitropic effect.

In contrast, enhancement of these same transporters would have a positive inotropic effect

References

Physiology of the cardiovascular system

Heart

Cardiac output	Cardiac cycle Cardiac output Heart rate Stroke volume Stroke volume End-diastolic volume End-systolic volume Afterload Preload Frank–Starling law of the heart Cardiac function curve Venous return curve Wiggers diagram Pressure volume diagram

Ultrasound	Fractional shortening = (End-diastolic dimension End-systolic dimension) / End-diastolic dimension Aortic valve area calculation Ejection fraction Cardiac index

Heart rate	Cardiac pacemaker Chronotropic (Heart rate) Dromotropic (Conduction velocity) Inotropic (Contractility) Bathmotropic (Excitability) Lusitropic (Relaxation)

Conduction	Conduction system Cardiac electrophysiology Action potential cardiac atrial ventricular Effective refractory period Pacemaker potential Electrocardiography P wave PR interval QRS complex QT interval ST segment T wave U wave Hexaxial reference system

Chamber pressure	Central venous Right atrial ventricular pulmonary artery wedge Left atrial ventricular Aortic

Other	Ventricular remodeling

Vascular system/
Hemodynamics

Blood flow	Compliance Vascular resistance Pulse Perfusion

Blood pressure	Pulse pressure Systolic Diastolic Mean arterial pressure Jugular venous pressure Portal venous pressure

Regulation of BP	Baroreflex Kinin–kallikrein system Renin–angiotensin system Vasoconstrictors Vasodilators Autoregulation Myogenic mechanism Tubuloglomerular feedback Cerebral autoregulation Paraganglia Aortic body Carotid body Glomus cell

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