Aneurysmal left main coronary fistula to RA in asymptomatic Patient with normal Left Ventricular function ( Answer to the weekly case challenges ) .

Q: An asymptomatic 32 year old woman with a murmur. What is it?

A: Aneurysmal left main coronary fistula to RA in asymptomatic pt, normal LV function.

•Learning Tips:

•Coronary artery fistulae (CAF) are rare cardiac malformations. Their prevalence has been reported at 0.1% to 0.2% of patients who undergo coronary angiography.

•Coronary artery fistulae are either congenital or acquired coronary artery abnormalities, that have different anatomical appearance; with varying degree of shunting (Qp/ Qs); and associated cardiac anomalies .

•Etiologies include high cardiac output state and congestive heart failure with shunting of blood into a cardiac chamber, great vessel, or other structures, bypassing the myocardial capillary network .

•If the fistula is large, the intracoronary diastolic perfusion pressure diminishes progressively .

•The coronary vessel usually attempts to compensate by progressive enlargement of the ostia and feeding artery.

•Nevertheless, myocardium beyond the site of the fistula’s origin is at risk for ischemia, most frequently evident in association with increased myocardial oxygen demand during exercise or activity .

•Although aneurysm formation is common in patients with coronary artery fistulae, giant aneurysms have rarely been reported.

•They are often asymptomatic and small, however, but rupture of an aneurysmal fistula can be fatal.

•Moreover, a coronary steal phenomenon can occur owing to blood shunting and perfusion away from the myocardium. This phenomenon can be manifested in the patient as angina pectoris.

•With time, the coronary artery leading to the fistulous tract dilates progressively, that in turn, may progress to frank aneurysm formation, intimal ulceration, medial degeneration, intimal rupture, atherosclerotic deposition, calcification, side- branch obstruction, mural thrombosis, and, rarely, rupture.

•Treatment is recommended in the presence of symptoms, a giant aneurysm, or progressive enlargement of fistulae.

•In cases of small and easily accessible fistulae, transcatheter closure could be considered.

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Silent Cerebral Infarct; associated with cardiac disease, procedures and other causes ! All in one

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Is his bundle pacing (HBP) a feasible alternative to RV pacing now or to CRT in future?

Dr. Nabil Paktin

The answer is, the Time and Market will prove it, NOT the Knowledge and Scholars!

Estimated that worldwide, about 1-3 million patients die annually due to a Lack of a Pacemaker.
 - By comparison, about 30.000 persons die annually from influenza, 1.6 million people died of HIV/AIDS in 2012.
Death from bradycardia is entirely preventable.

Right ventricular RV apical pacing has been the standard practice for patients requiring permanent ventricular pacing however long term RV apical pacing has its drawbacks.

 A prolonged PR interval results in reduced left ventricular filling, abnormal filling pattern, presystolic mitral regurgitation due to delayed and ineffective closure of the mitral valve. Prolongation of the PR interval results from cardiac conduction disease but may also be a marker of advanced structural heart disease associated with atrial electrical and structural remodeling of a long-standing RV apical or septal pacing.
 Prolongation of PR interval by itself independently associated with an increased risk of AF, increased mortality and heart failure hospitalization in the general population, in patients with CAD and in patients with left ventricular dysfunction.

Isolated RV pacing activates the interventricular septum before the LV lateral wall, seen as LBBB pattern on the ECG due to propagation of the electrical wave front away from the sternum result in LV dyssynchrony and mismatched timing between chamber walls, with deleterious effects on LV function and adverse clinical outcomes. Including heart failure and mortality. RV pacing-induced cardiomyopathy rates of up to 20% with frequent RV pacing among patients with preserved EF is reported.

RV apical pacing deleterious effects are as follows:

1,Altered left ventricular electrical and mechanical activation

2, Altered ventricular function

3, Remodeling

4, Cellular disarray

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Answer to an echocardiogram case challenge of the April?

Severe primary pulmonary hypertension with secondary RVH, dilation and dysfunction. Atrial septal aneurysm. Late contrast (after > 3 beats).
Saline microbubbes in left heart within 3 beats of arrival in RA = intracardiac shunt. 
Late = transpulmonary passage

IVC Filter Implantation for prevention of recurrent Pulmonary Embolism !

Pearls about DVT and Pulmonary embolism,

-Venous thromboembolism (VTE) is a serious preventable cause of morbidity & mortality in the world. -DVT & pulmonary embolism (PE) are distinct but related aspects of VTE. Being silent (80% DVT) and difficult to diagnose it poses great challenges in establishing diagnosis.-Higher incidence, underestimation of risk, low level of clinical suspicion, under-used prophylaxis with high fatality has made DVT a world wide cause for concern. -The immediate need of the hour is to have standard guidelines for management of DVT.

MECHANISM :

Based on Virchow’s triad; development of D.V.T. is primarily related to the stasis of blood flow, vascular wall damage, activation of clotting system and hypercoaguable state.
Blood passing through the deepest veins in calf or thighs flows relatively slowly than from a solid clot which becomes wedged in the veins.

-Estimates suggest that 60,000-100,000 Americans die of DVT/PE (also called venous 10 to 30% of people will die within one month of diagnosis.

-Sudden death is the first symptom in about one-quarter (25%) of people who have a PE.

-Among people who have had a DVT, one-half will have long-term complications (post-thrombotic syndrome) such as swelling, pain, discoloration, and scaling in the affected limb.

-One-third (about 33%) of people with DVT/PE will have a recurrence within 10 years.

-Only 1/3 of the hospitalized patients with risk factors for blood clots received preventive treatment .

-Without preventive treatment, Upto 60% patients who undergo total hip replacement surgery may develop D.V.T.

-Cancer patients undergoing surgical procedures have at least two times the risk of post operative D.V.T. and greater than three times risk of fatal P.E. than non cancer patients undergoing similar procedure.

-In elderly, D.V.T. is associated with 21% one-year mortality rate and P.E. is associated with 39% one-year mortality rate.

-P.E. is the leading cause of maternal death associated with childbirths.
A woman’s risk of developing DVT is six times greater when she is pregnant.
.

-Evaluation and proper management is essential to decrease the burden of V.T.E.
-While surgical patients seem to draw attention of medical fraternity; it needs to be remembered that non-surgical medical patients are at an equal or at higher risk of developing V.T.

PREDISPOSING FACTORS :

Patient Factors :

-Age> 40 risk increase exponentially with age

-Obesity (BMI > 30 kg/ m2) 

-Varicose veins or venous thrombophlebitis

-Previous D.V.T.

-Oral contraceptives & Hormone replacement therapy ; oestrogen is responsible for D.V.T.

-Pregnancy : due to 

(i) Hormonal Changes

(ii) Pressure on veins by fetus

-Highest incidence in puerperium especially just after childbirth

-Dehydration : increase blood viscosity

Immobility : Stasis of blood

Long distance travel : due to (i) Inactivity  (ii) Dehydration

due to these factors blood becomes more sticky specially if journey is for more than 5 hrs. 
          - Blood disorders  

 

 

Myth of ST-elevation in AVR and ACS ! , If you hear hoofbeats think horses not zebras And if you see hoofbeats of ZEBRA not to thinks about any Horse !

If you find ST-elevation in AVR and ST-segment change in other leads , first see these doubts on Echo before thinking about ACS or taking into Cath Lab, if all walls contracting well then ACS is ruled out.

ST elevation in aVR is not entirely specific to LMCA occlusion.
ST Elevation in aVR may also be seen with:
-Proximal left anterior descending artery (LAD) occlusion
-Severe triple-vessel disease (3VD)
-Diffuse subendocardial ischaemia – e.g. due to O2 supply/demand mismatch,

Mechanism of ST elevation (STE) in aVR

-Lead aVR is electrically opposite to the left-sided leads I, II, aVL and V4-6; therefore ST depression in these leads will produce reciprocal ST elevation in aVR.
-Lead aVR also directly records electrical activity from the right upper portion of the heart, including the right ventricular outflow tract and the basal portion of the interventricular septum. Infarction in this area could theoretically produce ST elevation in aVR.
-ST elevation is aVR is postulated to result from two possible mechanisms:

-Diffuse subendocardial ischaemia, with ST depression in the lateral leads producing reciprocal change n aVR  most likely).
Infarction of the basal septum, i.e. a STEMI involving aVR.

BUT THESE ALL ARE ECG concepts , ECHO will SHOW YOU THE ECG IN REAL LIFE .

:)

What is grave sign or “tombstone” ST segment elevation of MI ( Tombstoning ECG =grave prognosis)

Tombstoning ST elevation myocardial infarction can be described as a STEMI characterized by tombstoning ST-segment elevation. This myocardial infarction is associated with extensive myocardial damage, reduced left ventricle function, serious hospital complications and poor prognosis. Tombstoning ECG pattern is a notion beyond morphological difference and is associated with more serious clinical results.

It appears that a sudden occlusion of a coronary artery supplying a large area of unprepared myocardium; i.e. myocardium not protected by collaterals or ischemic preconditioning, results in complete transmural injury rapidly progressing to complete infarction, resulting in this characteristic ECG pattern. The extensive nature of the myocardial infarction and the resultant left ventricular damage and dysfunction may explain the higher risk of complications and mortality associated with this finding. The higher BNP levels on presentation in patients with tombstone STEMI seem to support the extensive nature of the myocardial damage associated with this ECG finding.