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.

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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.

Can antiplatelet agent be considered as an alternative to OAC in SPAF? Can we combine the Oral anticoagulants with anti-platelets in SPAF?

Can antiplatelet agent be considered as an alternative to OAC in SPAF?

In terms of stroke prevention in AF, the bottom line is effective stroke prevention means oral anticoagulation therapy and these days it can either mean a NOAC (non vit. K oral anticoagulant) or Vit.K antagonist (VKA) e.g. Warfarin because that is where the evidence is clearly there which shows that OAC harpy prevents stroke. Aspirin or anti-platelet therapy had been tested in SPAF (stroke prevention in Atrial fibrillation), and the evidence suggests no significant benefits, there is however evidence of harm i.e. increase in the risk of both major and intracranial bleeding. NICE guidelines in UK, in 2014 which also undertakes a cost effectiveness analysis stated that not only is aspirin ineffective but it is actually not safe and certainly not cost effective. In net clinical benefits for aspirin in SPAF is essentially neutral or trending towards harm. In short, aspirin mono-therapy should be used as Mono-therapy in SPAF.

Can we combine the Oral anticoagulants with anti-platelets in SPAF?

Anti-platelet therapy can be combined with oral anticoagulant therapy essentially in a situation of the patient with AF possesses ACS or undergoes coronary intervention including coronary stenting. In patient with stable vascular disease essentially in majority of patients with AF there is no demonstrated benefit to add anti-platelet therapy to oral anticoagulant therapy because the available data shows that there is no benefit in terms of stroke reduction, morality or myocardial infarction, however, what you do see is a significant increase in major bleeding as well as significant increase in intracranial bleeding when anti platelet therapy is combined with oral anticoagulation.

So in short do not combine anti-platelet therapy and oral anticoagulant therapy in majority of patients of AF as there is little evidence of benefit, there is certainly strong evidence of harm in these patients.

This combination therapy should be reserved when there is a necessity to have associated anti-platelet therapy most commonly after an ACS or a coronary stent intervention.

What is Fragmented QRS complex ? " QRS fragmentation vs. Q wave importance"

BioResorbable Stents (BRS) Pearls / Updates on BVS ( BioVascular scaffolds )