Monday, July 21, 2014

The Vicious Cycle of Atrial Fibrillation and Heart Failure !


A case of Reverse-Typical Atrial Flutter ! Answer about ECG case challenge (dated:15th/july/14)

A 24 years girl reffered from Vascular surgery to ICCU due to Dilated Cardiomyopathy (EF=30%) , and recently B/L Femoral embolectomy and Rt.Leg Fasciotomy done and there is also H/O right sided hemiparesis due to thromboembolic stroke , BP 80/50.
According to researches results and references :
1- Atrial Flutter is a supraventricular arrhythmia with regular atrial rate of 300+_ 50 beats per minute  ( here is the same ) 
2- Atrial Fibrillation from atrial flutter beside of fine and coarse F waves , differ by regular ventricular rhythms . ( here is the same ) 
3- There was clear cause for that , there is DCMP with EF=30% . this plus atrial flutter lead to thromboembolic stroke ! Af Vs. AFL have the same thromboembolic risk . 
4- there is no bifascicular block because we can say bifascicular block with RBBB not LBBB. 
5- Typical is associated with negative (f) waves in II, III, AVF- while reversed typical is accompanied with Positive (f) waves ( here the same ) .Once should be noted leads II, III, and aVF is more powerful indicator of Typical Vs. Atypical than Lead V1, it is believed that even in the absence of V1 for confirming of typical or atypical , the inferior leads are mostly trusted .  
6- by palpation we could find fixed ventricular rate . and etc...
Therefore , we can say , this is a case of Reverse-Typical Atrial Flutter with 4:1 AV conduction ration , and LBBB with atrial rate of about 300 and ventricular rate of about 66 beats per minute .

Saturday, July 19, 2014

What does PR-Interval indicate on ECG truly ?


The period of time from the onset of the P wave to the beginning of the QRS complex is termed the P-R interval, which normally ranges from 0.12 to 0.20 seconds in duration.
The term “PQ interval” is preferred by some electrocardiographers because it is the period actually measured unless the Q wave is absent.
In contrast to common and old believe which PR interval represents the time take for the signal to move across from SA-node to AV node ,the PR interval spans the time required for the propagating impulse to advance from the atria through the AV node, bundle of His, bundle branches, and the system of Purkinje fibers until the ventricular myocardium begins to depolarize .It does not include the duration of conduction from the SA node to the right atrium (SA conduction).

Friday, July 18, 2014

Troponin T or troponin I and Why ?! In a suspected patient of ACS , if you have one option , either to select Troponin-I or Troponin-T , which one do you prefer ?

Written by : Dr.Nabil Paktin,MD.,F.A.C.C.


With the emergence of cardiac troponin T (cTn T) in the late 1980s and troponin I (cTn I) in the early 1990s, the diagnosis of Myocardial Infarction become easy .

Figure 1 
The mechanism by which cTnI and cTnT are released into circulation has not been well  elucidated but posssibilites suggested include normal turnover of myocardial cells , apoptosis , cellular release of cTn degradation products , increased cellular wall  permeability , formation and release of membranous blebs and myocyte necrosis .Although assays for cardiac troponin T (cTnT) and cardiac troponin I (cTnI) exhibit similar clinical performance in patients with acute coronary syndromes for diagnosis and risk stratification, there are differences in the release and clearance of these proteins from damaged myocytes.

         
In certain situations , troponin I and Troponin T results may differ , and therefore these two assays cannot be used interchangeably .

1- After Cardiac surgery , significantly different results can be expected from these two assays , with troponin I reaching much higher levels than Troponin T .

2-Different epitopes/antibody recognition sites will result in difference in the detection of complexes and degradation products as well as Differences in phosphorylation , reduction and oxidation is also there .


3- Heparinized plasma samples allow more rapid analysis than serum samples, but preliminary studies showed lower cardiac troponin T (cTnT) results in plasma. negatively charged polyanions on heparin bind to positively charged troponins. To the best of our knowledge, loss of troponin T in heparin sampling tubes has not previously been published. The early phase of myocardial damage, troponin T occurs mainly as a “free cytosolic” form; in the later phase, it occurs in the “structurally bound” form and fragments . Troponin I is primarily released into plasma as a binary complex with troponin C and later occurs as a distribution of a variety of forms . We conclude that heparin decreases the measured concentrations of cardiac troponins, probably by binding to troponins and reducing their immunoreactivities. The magnitude of the decrease depends on the distribution of different troponin forms in circulation during and after myocardial damage and on analytical antibodies used in different troponin assays.Figure 1 .

For Further Reading Please Click here 

Wednesday, July 16, 2014

Simple changes in ICU can help heart attack patients: Study

The new study shows for the first time that interrupting diurnal rhythms impairs healing immediately after a heart attack, said Prof. Tami Martino of the Department of Biomedical Sciences.
Researchers already knew that circadian rhythms, or day-night cycles, can affect timing of a heart attack. This is the first study to show the importance of circadian rhythms during the few days after an attack.
The study led by U of G scientists appears this week online in Circulation Research journal.
 "We have devised a simple way to better practise medicine to improve the outcome from heart attacks by considering normal circadian rhythms," she said.
She and PhD student Faisal Alibhai conducted the study with clinician collaborators, who are already looking at ways to use the results to change practices in intensive care units (ICU). "It has an immediate life application," said Martino.Hospital ICUs are busy places at night, with noise, light, nursing and medical procedures, and other interruptions that disturb acutely ill patients.The team induced heart attacks in mice, and then compared rodents held under normal light and dark cycles with others whose diurnal cycles were disrupted for five days after the attacks.
Early heart repair and remodeling were impaired in the disrupted mice. Diurnal disruptions interfered with their normal inflammatory and immune responses crucial for scar formation and healing."These mice were likely to go more quickly to heart failure," said Martino. "Disrupting circadian rhythms for the first few days after a heart attack worsens the disease outcome."The first five days after a heart attack are crucial for proper scar formation, removal of dead tissue, proliferation of new cells and growth of blood vessels in the heart.
Journal Reference:
  1. F. J. Alibhai, E. V. Tsimakouridze, N. Chinnappareddy, D. C. Wright, F. Billia, L. O'Sullivan, W. G. Pyle, M. J. Sole, T. A. Martino. Short Term Disruption of Diurnal Rhythms Following Murine Myocardial Infarction Adversely Affects Long Term Myocardial Structure and Function. Circulation Research, 2014; DOI: 10.1161/CIRCRESAHA.114.302995

Sunday, July 13, 2014

Normal and dysfunctional endothelium

Since the landmark study of Furchgott and Zawadski in 1980, it has become well known that endothelium plays a critical part in modulating vascular tone in large conduit arteries as well as in the microcirculation.
Several studies have shown that the vasoactive effects of acetylcholine, serotonin, norepinephrine (noradrenaline), thrombin, substance P, adenine nucleotides, bradykinin, and endothelin result from a balance between their direct vasoconstrictor effects on the vascular smooth muscle and their indirect endotheliumdependent vasodilator effects.
When endothelium is intact and healthy, a net vasodilator effect predominates; however, when endothelium is structurally damaged or functionally abnormal, vasodilator responses to these endothelium-dependent
vasodilators are attenuated, and paradoxical vasoconstriction can occur (Fig. below).

Saturday, July 12, 2014

Green tea, coffee may reduce stroke risk

Researchers have discovered a link between stroke  development and coffee and green tea consumption. A 
study published in Stroke shows that green tea and coffee  may help lower the risk of having a stroke.
The researchers asked 83,269 Japanese adults, ages 45–74  years without cardiovascular disease or cancer, about their  green tea and coffee drinking habits and tracked them for 
an average 13 years. Green tea and coffee consumption was  assessed by self-administered food frequency  questionnaire at baseline. They found that the more green tea or coffee people drink, 
the lower their stroke risks.

• People who drank at least one cup of coffee daily had  about a 20 percent lower risk of stroke compared to   those who rarely drank it.
• People who drank two to three cups of green tea daily  had a 14 percent lower risk of stroke and those who had  at least four cups had a 20 percent lower risk, compared  to those who rarely drank it.
• People who drank at least one cup of coffee or two cups  of green tea daily had a 32 percent lower risk of 
intracerebral hemorrhage, compared to those who  rarely drank either beverage. (Intracerebral hemorrhage  happens when a blood vessel bursts and bleeds inside  the brain. About 13 percent of strokes are hemorrhagic.)

Conclusions: Higher green tea and coffee consumption  were inversely associated with risk of CVD and stroke in  general population.


Source: Green tea, coffee may help lower stroke risk 
[Internet]. [published 2013 Mar 14; cited 2013 Nov 27]. 
Available from: http://newsroom.heart.org/news/greentea-coffee-may-help-lower-stroke-risk