Focused Update on SIHD Guideline Released

The ACC and the American Heart Association, along with several other partnering societies, have released an updated guideline for the diagnosis and management of patients with known or suspected stable ischemic heart disease (SIHD), including those with new-onset chest pain or stable pain syndromes.

The focused update, published July 28 in the Journal of the American College of Cardiology,  adds a new section specifically addressing the role of coronary angiography for the diagnosis of coronary artery disease (CAD) in patients with suspected SIHD, and includes several new or updated recommendations for treatment options, as well as CAD revascularization. The new section on coronary angiography includes four new recommendations, including a "Class I" recommendation for use "in patients with presumed SIHD who have unacceptable ischemic symptoms despite guideline-directed medical therapy and who are amenable to, and candidates for, coronary revascularization." Despite its certain "shortcomings and potential complications," the guideline writing group noted several areas where coronary angiography can be used to:

• Ascertain the cause of chest pain or anginal equivalent symptoms
• Define coronary anatomy in patients with ‘high-risk' noninvasive stress test findings as a requisite for revascularization
• Determine whether severe coronary artery disease may be the cause of depressed left ventricular ejection fraction
• Assess for possible ischemia-mediated ventricular arrhythmia
• Evaluate cardiovascular risk among certain recipient and donor candidates for solid-organ transplantation
• Assess the suitability for revascularization of patients with unacceptable ischemic symptoms (i.e., symptoms that are not controlled with medication and that limit activity or quality of life)

They also suggest that coronary angiography may be helpful if initial stress testing is inconclusive or has conflicting results.

In terms of SIHD treatment, the guideline writing group updated the recommendation for chelation therapy from "Class III: No Benefit" to "Class IIb" indicating the usefulness of chelation therapy is uncertain for reducing cardiovascular events in SIHD patients. "Although disodium ethylene diamine tetraacetic acid is approved by the U.S. Food and Drug Administration for specific indications, such as iron overload and lead poisoning, it is not approved for use in preventing or treating cardiovascular disease," they said. However, the writing group chose not to update the 2012 recommendation stating enhanced external counterpulsation (EECP) may be considered to help relieve refractory angina in SIHD patients. After re-examining the scientific evidence the group noted that, "in general, existing data, largely from uncontrolled studies, suggest a benefit from EECP among patients with angina refractory to other therapy." They went on to say that "additional data from well-designed randomized controlled trials are needed to better define the role of this therapeutic strategy in patients with SIHD."

CAD revascularization was another area of renewed focus for the writing group. The updated guideline includes a new "Class I" recommendation for a Heart Team approach to revascularization in patients with diabetes mellitus and complex multivessel CAD. In addition, the 2012 Guideline provision "probably" recommending coronary artery bypass graft surgery (CABG) over percutaneous coronary intervention (PCI) to improve survival in patients with multivessel CAD and diabetes mellitus, was updated to say "CABG is generally recommended in preference to PCI to improve survival in patients with diabetes mellitus and multivessel CAD for which revascularization is likely to improve survival … provided the patient is a good candidate for surgery." The writing group suggests going forward that future research may be facilitated by including a field in the ACC's CathPCI Registry and the Society of Thoracic Surgeons database to identify cases "turned down" for the alternative revascularization strategy.

Treatment Delayed is Treatment Denied !

 In ACS: Loss of Time = Loss of Cardiac Myocyte

Loss of Cardiac Myocyte = Loss of Life or Quality of Life !

Acute Left Ventricular Remodeling Following Myocardial Infarction :The role of myofibroblasts !

All Complete AV Block into one Picture !

Answer to ECG case challenge dated ( 23/7/14) A 62 years old diabetic man with sudden onset dyspnea on exertion , BP -100/60, bibasilar lung crackles .

What is Propofol-Infusion Syndrome ?

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 .

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).

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 

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

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).

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