Why cardiac chest pain is common in morning than night ? and which type of Cardiac chest pain relievd by physical exertion?
#1. Circaridan Rhythm and Chest Pain
Mammalian daily rhythms are regulated by a pacemaker within the suprachiasmatic nuclei of the hypothalamus, called the circadian clock. This biological system consists of a combination of genes and proteins that behave in a cyclical way following a 24-hour pattern. It is not only governed by endogenous factors, but also by environmental stimuli, the most important of which is the dark-light cycle. Chronobiological rhythms have been observed for many physiological parameters such as body temperature, blood pressure, hormone levels, etc. In fact, most of the biological ‘drivers’ of human life appear to follow a diurnal pattern A marked circadian variation of disease onset has been reported with a maximum events occurring between 09.00 and 10.00 in the morning and a minimum events of between 23.00 and 24.00 at night.
Myocardial infarction was approximately four times more likely to occur between 08.00 and 09.00 in the morning than between midnight and 01.00. Hematological factors (e.g., increases in aggregability of platelets), vascular endothelial factors (e.g., increase in vascular tone), autonomic factors (e.g., release of catecholamines), and hemodynamic factors (e.g., morning surge of blood pressure and shear forces) have all been implicated in these adverse cardiovascular events which is activating during morning time.
The suprachiasmatic nuclei controls the biochemical, metabolic, physiological, and behavioral processes of mammals, including the cardiovascular system. The cardiovascular system follows circadian variations driven by humoral signs. Cortisol and epinephrine levels increase during the morning period and fall during sleep, and both are considered one of the main humoral signs that connect the circadian clock and peripheral system activity. Aldosterone and plasma renin activity also follow circadian patterns, being higher in the morning and modulating the cardiovascular system. The circadian clock also controls melatonin production at the pineal gland. This hormone influences the circadian rhythm by a negative feedback mechanism, regulating circadian physiology. Simultaneously, melatonin influences cardiovascular pathophysiology by a double mechanism, binding melatonin receptors present throughout the vascular system and heart, and acting directly as an antioxidant factor. Heart rate and blood pressure oscillate throughout the day in phase with these circulating factors, being higher in the morning and decreasing during the evening.
Endogenous thrombolytic activity and platelet aggregability also follow a circadian pattern. The plasma levels of fibrinogen and plasminogen activator inhibitor-1 activity increase between 6 am and noon, whereas antithrombin levels and the activity of tissue-type plasminogen activators decrease during the morning.This fact suggests a thrombogenic natural status during the first hours of the day that turns into a physiological pro-fibrinolytic status in the evening hours.
There are several clues to the factors responsible for this phenomenon. Platelets aggregation has been reported to be more responsive during morning. Conceivably, early morning hypercoagulability could enhance the intracoronary thrombosis and there by increases the risk of major advance cardiac events (MACE). Another important factor in the pathogenesis of the increased morning incidence of ischemic cardiac events may be the early morning increase of arterial pressure.The increased arterial blood pressure, increases the myocardial oxygen demand that leads to the increased vulnerability of the myocardium to ischemia, secondly the increase in arterial blood pressure could enhance the risk of plaque fissure that has been shown to occur rapidly before myocardial infarction. Several other factors for e.g. hormonal changes or increase in coronary artery tone may also play a role in the pathogenesis of this phenomenon. It has been proposed that in a number of cases, sudden cardiac death is the result of primary arrhythmic event. Such fatal arrhythmias are more likely to occur in the morning since increased activity of the sympathetic nervous system at that time. which in turn may increase electrical instability and subsequent conduction defects.
#2.Warm up Angina ( second wind or walk through ) angina
The traditional view is that angina is the result of an imbalance between the supply and demand of the myocardium for blood. The traditional explanation of warm up angina has therefore been that myocardial blood flow is enhanced on second effort by the opening of collateral channels (ie, collateral recruitment), and vasodilatation of the diseased artery or subtended vascular bed, or both. It is postulated that the collateral coronary channels may dilate slowly, and in the other it may be the larger coronary vessels which maintain a reduced capability of dilatation at their stenotic points.
A large increase in flow would result from only a small increase in diameter, since by Poiseuille’s law the flow increases as the fourth power of the radius.
However, the observation of increased myocardial resistance to ischemia after a brief episode of ischemia, known as ischemic preconditioning, has increased the understanding of warm up or second wind angina. In contrast to the traditional view, ischemic preconditioning does not depend on an increase in myocardial blood flow, but is caused by an increase in the intrinsic resistance of the heart to ischemia.
The term ‘‘ischemic preconditioning’’ and referred to it as myocardial adaptation to ischemic stress induced by repetitive brief periods of ischemia and reperfusion. . Not all time combinations and durations of ischemia and reperfusion will trigger the preconditioning phenomenon and afford myocardial protection. Ischemic preconditioning can be induced by a period of ischemia as short as 3 min, followed by a minimum of 1 min of reperfusion , but a brief 1–2 min period of ischemia followed by subsequent reperfusion has no protective effect.
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