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.

Recurrent Vasospastic Myocardial Infarctions and Hand Necrosis

A 30-year-old male smoker presented to the emergency department with anterior ST-segment elevation myocardial infarction. Primary percutaneous coronary intervention performed via the right radial artery showed an ostial thrombotic subocclusion of the left anterior descending artery (Figure 1A, black arrow) successfully treated with 2 drug-eluting stents under abciximab perfusion.

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

What is Early Repolarization Syndrome ? Is it Benign or malignant ? Definition/Classification/ Risk factors

PCI versus early thrombolysis For patients with an ST elevation myocardial infarction

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.

For More Reading Please Click Here the Link  Read More Below !↙

Atrial Flutter !

How a venous/coronary artery bypass graft fails ? (What is neointimal hyperplasia ) ?

The main limitation of coronary artery bypass grafting (CABG), when the saphenous vein is used as a conduit, is poor long-term vein graft patency. Fiveyear failure rates are 30–50% and have remained unchanged despite rapid development of pharmacological treatments and technologies.
Perhaps the most important change following vein grafting is the exposure of saphenous vein to the arterial circulation. In the venous circulation saphenous vein is subjected to low pressure, non-pulsatile flow and a shear stress of around 0.2 dyne/cm2
Following grafting the vein is exposed to high pressure, pulsatile flow and a shear stress of approximately 3-6 dynes/cm 2. In addition to increased shear stress the vein is subjected to a variety of other new haemodynamic forces, including radial and circumferential deformation.

The another main reason for vein graft occlusion, especially in the mid-term, is neointimal hyperplasia (NIH).
Following vein grafting there is rapid deposition of leukocytes, platelets and other blood components. . These accumulating cells and blood components may have an important influence on the later development of intimal hyperptasia.In the experimental situation inhibiting leukocyte accumulation using an antibody to CD4 results in a reduction in the development of intimal hyperplasia, 
 while reduction in platelet aggregation using an antibody to GP IIb-IIIa has been shown to reduce the incidence of restenosis following coronary angioplasty in vivo. 
 Monocytes is also playing  important role. Studies of excised vein graft stenoses has demonstrated an abundance of proliferating monocytes and macrophages in the intima of these lesions. 
Leukocytes can release cytokines, oxygen-derived free radicals and lysosomal proteinases, which, by direct effects on smooth muscle cells and also modulation of endothelial products, e.g. inactivation of nitric oxide, may influence smooth muscle cell proliferation and migration. 
 Similarly deposited platelets release smooth muscle mitogens, such as platelet derived growth factor, which encourage smooth muscle cell proliferation and migration into the intima. 
 Studies in cultured cells have demonstrated that haemodynamic forces have an important influence on the endothelial expression of molecules controlling leukocyte and platelet adhesion. Thus it is tempting to explain the association between haemodynamic forces and vein graft thickening by their effect on the accumulation of blood elements.  
It is well-known that  aortocoronary grafts fashioned from internal mammary artery or radial artery are much more durable than saphenous vein grafts and it is of note that SMCs derived from internal mammary artery proliferate less than SMCs from saphenous vein.
 There are significantly higher activity of phosphatase and tensin homolog (PTEN) in the smooth muscle cells of the internal mammary artery than in the saphenous vein.
In summary one can say that :
In vein-graft failure  various factors pathophysiologiclly are involved , including PTEN, matrix metalloproteinases, and tissue inhibitor of metalloproteinases, in uncontrolled proliferation and migration of smooth muscle cells towards the lumen, and invasion of the graft conduit.