Saturday, April 8, 2017

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 .
:)

Monday, March 13, 2017

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.

Monday, February 27, 2017

Recurrent Vasospastic Myocardial Infarctions and Hand Necrosis

Two days later, the patient developed an inferior ST-segment elevation myocardial infarction and the repeated percutaneous coronary intervention via the same vascular access revealed a subocclusion of the previously normal mid–right coronary artery (Figure 1B, black arrow). Intravascular optical coherence tomography confirmed the angiographic suspicion of focal vasospasm (Figure 1C), showing a concentric narrowing without atherosclerosis, dissection, or thrombus.
After ineffective intracoronary nitroglycerin and verapamil injection, balloon angioplasty without stenting permitted the resolution of spasm and the alleviation of symptoms. Although drug tests were negative, the patient admitted occasional consumption of cocaine and methylamphetamine. He was discharged on oral calcium-channel blocker and dual antiplatelet therapy and the cardiac rehabilitation was uneventful.
Three months later he developed severe right hand ischemia due to extensive spastic and thrombotic occlusions of the forearm and finger arteries (Figure 1D, black arrows) refractory to vasodilators, fibrinolytic agents, and endovascular revascularization. Despite fasciotomy (Figure 1E), transradial amputation was required due to extensive necrosis. The vascular histology showed an intimal mononuclear infiltration. A cocaine-associated thromboangiitis obliterans was retained as final diagnosis.
As showed in our case, the cocaine-derived cardiovascular risks are present not only in the consumption period but could occur weeks or months later and should be considered as risk factors for dramatic outcomes.



Reference :
JACC: Cardiovascular Interventions
Volume 10, Issue 2, January 2017

Sunday, January 22, 2017

What is Free floating ball thrombus ( FFBT)? , A case of Moderate MS , mild MR and mildly dysfunctional LV and AF

Wood who first applied the term ball valve thrombus to this entity in year 1814, describe autopsy finding in 15 year old girl with rheumatic mitral valve stenosis and syncope.

Left atrial ball valve thrombus is an important pathology and left atrial (LA) ball thrombus is a rare disorder. It is most often associated with rheumatic mitral valve stenosis. However it has been reported without mitral stenosis also.
This phenomenon is seen in 17% of patients with severe mitral stenosis, and the risk doubles with atrial fibrillation.

 However, left atrial ball thrombi have rarely been reported in patients who have had no mitral valvular disease. A left atrial ball thrombus in non-rheumatic atrial fibrillation was first described in 1992.


The restricted mitral orifice encloses the free-floating thrombus in the LA. Ball valve thrombus in the left atrium (LA) is a spherical clot which is freely mobile and intermittently occludes the mitral valve orifice.

There is a potential for fatal systemic emboli or mitral valve orifice occlusion that may result in sudden death.

Almost all patients with a left atrial free floating ball thrombus have atrial fibrillation. Concomitant cardiac diseases besides of   mitral stenosis are post mitral valve replacement, myocardial infarction, myocarditis, hypertrophic cardiomyopathy and infective endocarditis.


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