Welcome to my blog which is dedicated to sharing and analyzing cardiology trends and information ranging from the basics, all the way to new, cutting edge discoveries. In this site you will find lectures, journal reviews, guidelines, researches, news ,CMEs and articles. Students and professionals alike are invited. I hope you will enjoy reading and sharing your valuable perspectives too. "Dr.Nabil Paktin , MD.,F.A.C.C."
Thursday, March 19, 2015
Sunday, March 15, 2015
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.
.
Why there is thrombocythopenia in Endocarditis ?
#1-
rare causes -one type is Nonbacterial thrombotic endocarditis (Marantic
endocarditis) - if this can be seen with thrombocytopenia then called
-Para-neoplastic syndrome. Cancer may affect cellular elements of the
blood as well as coagulation system , resulting in a wide range of para
neoplastic syndrome . In this cases thrombocytopenia is rare but
thrombocytosis which results from IL-6 and thrombopoietin release which
may play a role in hypercoagulable state and may present as
non-bacterial endocarditis in either cases.
#2- is more common : Infective endocarditis (IE) is a life threatening disease caused by a bacterial infection of the endocardial surfaces of the heart. It is typified by the formation of septic thrombi or vegetative growth on the heart valve. Typically, both platelets and fibrin are deposited on exposed extracellular matrix proteins as part of the normal response to damage of the endocardium . However, this sterile platelet-fibrin nidus facilitates colonisation of the endocardium by bacteria in the bloodstream . Following attachment, bacteria can recruit platelets from the circulation inducing platelet activation and platelet aggregation. !! S aureus adheres to platelets, leading to platelet activation and aggregation,platelet consumption, and eventually thrombocytopenia.
#3- Initial studies focused on secreted mediators of platelet activation such as alpha-toxin, which accelerates thrombin generation. Later studies focused on Clf A and fibronectin-binding protein A as the dominant surface proteins mediating platelet activation.Also, Clf A has been shown to be a virulence factor for endocarditis.This platelet activation process requires 2 mechanisms of S aureus binding to platelets: by a fibrinogen or fibronectin bridge to the platelet integrin GPIIb/IIIa and an immunoglobulin bridge to the Fc-γ-RIIa receptor.
#2- is more common : Infective endocarditis (IE) is a life threatening disease caused by a bacterial infection of the endocardial surfaces of the heart. It is typified by the formation of septic thrombi or vegetative growth on the heart valve. Typically, both platelets and fibrin are deposited on exposed extracellular matrix proteins as part of the normal response to damage of the endocardium . However, this sterile platelet-fibrin nidus facilitates colonisation of the endocardium by bacteria in the bloodstream . Following attachment, bacteria can recruit platelets from the circulation inducing platelet activation and platelet aggregation. !! S aureus adheres to platelets, leading to platelet activation and aggregation,platelet consumption, and eventually thrombocytopenia.
#3- Initial studies focused on secreted mediators of platelet activation such as alpha-toxin, which accelerates thrombin generation. Later studies focused on Clf A and fibronectin-binding protein A as the dominant surface proteins mediating platelet activation.Also, Clf A has been shown to be a virulence factor for endocarditis.This platelet activation process requires 2 mechanisms of S aureus binding to platelets: by a fibrinogen or fibronectin bridge to the platelet integrin GPIIb/IIIa and an immunoglobulin bridge to the Fc-γ-RIIa receptor.
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Friday, March 6, 2015
Angina with Normal Coronaries
Evidences have been shown that about 30% patient’s who
admitted due to chest pain , Coronary
angiograms show normal coronaries and 60% of post PTCA patients’ show TMT
positive for inducible angina .
Normal or nonobstructive coronary disease at angiography is
not uncommon and occurs in 10% of women presenting with ST segment elevation
myocardial infarction compared with 6% in men.
Randomized placebo-controlled studies have demonstrated that
tricyclic antidepressants, beta-blockers, ACE inhibitors, L-arginine, statins
and exercise may relieve symptoms, vascular dysfunction, or both, however,
long-term studies evaluating cardiac event rates need to be performed.
Features of chest pain may suggest:
- Non-cardiac chest pain
- Atypical angina including vasospastic angina
- Cardiac syndrome X
Normal coronary angiograms
do not exclude the presence of myocardial ischemia in women. Coronary disease
and chest pain, which may occur despite normal routine angiograms, include
variant angina and syndrome X. Differentiation between these 2 entities may not
be possible without further specialized provocation tests.
Important to differentiate non-cardiac chest pain from other
2 conditions:
- if angiographic appearance are suggestive of
non-obstructing lesions and stress imaging techniques identify an extensive
area of ischemia then :
- Intravascular USG of assessment of coronary flow reserve
or fractional flow reserve may be considered to exclude missed obstructive lesions.
- Intra coronary ACETYLCHOLINE or ERGONOVIE may be
administered during coronary arteriography .
Link between high-fat diet and cardiomyopathy, heart faiulre and early death
Evidences suggest that in healthy individuals SIRT6 suppresses IGF signaling–related genes by binding and silencing expression from AP1-dependent promoters, and this contributes to metabolic homeostasis and the maintenance of a healthy heart. Low expression of SIRT6 possibly caused by a high-fat diet, sedentary lifestyle and/or genetics results in reduced SIRT6 silencing, and overexpression of IGF and possibly also of other AP1-dependent genes, thus promoting cardiomyopathy, heart failure and early death.