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 )

What is intra cardiac blood cyst ?

Blood cyst in the heart is a very  rare finding and was first reported by Elasser in 1844. The cysts are most commonly present on the supporting structures; atrioventricular valves, accounting for 96% of the cysts in infants, and are less often present on pulmonary and aortic valves.

Histologically, it is thin-walled and normally lined by cobblestone-shaped endothelial cells and does not contain any tumorous cells.

Blood cysts are often asymptomatic, small and congenital. The cysts regress spontaneously in most patients and are consequently rare in adults, there are some cases reported in contrast.   Cyst growth potential complications include valve dysfunction, left ventricular outflow tract obstruction, and embolic stroke have been documented.

In differential diagnosis  primary cystic tumor such as hemangioma or myxoma should be taken into account and the right-sided cystic mass includes

aneurysmatic atrioventricular septum, cavitating thrombus, abscess formation as a process  of endocarditis, hydatid cyst, and blood cyst.

However, absence of intracystic calcification, homogenous pattern of cystic

fluid, relation to the tricuspid valve, and clinical history strongly suggested a blood cyst in our patient.

Echocardiography indicated the cystic nature of the tumor which is highly mistaken with cardiac hydatidosis. However, cardiac MRI was important for its diagnosis.

Hydatid cysts exhibit a different behavior under MRI, being a

a round homogeneous image is observed with signs of bleeding (iso- or hyperintense in T1 and iso- or hypointense in T2) with no uptake of IV contrast media, which indicates its hematic and cystic nature

Because of the cyst’s location, a myxoma could be suspected, but myxomas tend to be heterogeneous, and although some may exhibit a more homogeneous behavior, they always exhibit contrast uptake, being solid lesions.
 

A chronic thrombus may have similar intensity in T1 and T2, but its round morphology, its well-defined margins, the presence of a tiny pedicle, and its cystic nature as revealed by MRI and echocardiography do not support this diagnosis.

Although a cardiac blood cyst is a very rare finding, it can

be diagnosed using cardiac MRI and it should be included in

the differential table of masses inside heart cavities.

There are several purposed mechanisms for formation of cystic mass ,however, it is believed that invagination at crevices of the valve surface into stroma by high ventricular pressure may result in blood-filled cyst formation. Subsequently, the mouths of the crevices may fuse to form a closed cyst.

The followings are hypotheses :

The first is that blood cysts are formed during valve development as a result of blood being pressed and trapped in crevices that are later sealed off.

The second hypothesis is that blood cysts are the result of hematoma formation in the subvalvular region secondary to the occlusion of small vascular branches of end arteries due to inflammation, vagal stimulation, anoxia, or hemorrhagic events.

The third hypothesis involves possible heteroplastic changes in the tissue that comes from primitive pericardial mesotheli­um.

The fourth and fifth hypotheses are that these blood cysts simply represent ectatic or dilated blood vessels in the valve or that they represent angiomas.

However, there is still no con­sensus regarding the development of blood cysts.

Dencker et al suggested that a conservative approach in asymptomatic patient with minor cyst, and surgical resection should be considered if symptoms exist or if the cysts lead to any cardiac dysfunction.

References

1)        Michelena HI, Mulvagh SL, Schaff HV, Enriquez-Sarano ML, Klarich KW. A heart-shaped mass inside a heart: echocardiographic diagnosis, pathology, and surgical repair of a flail tricuspid valve caused by a large blood-filled cyst. J Am Soc Echocardiogr 2007;20:771.e3–6.

2)       Jose VJ, Gupta SN, Jose S, Chacko B, Abraham PK, Abraham OC et al. Blood-filled cysts of heart. Indian Heart J 2004;56:174–5.

3)        Shing M, Rubenson DS. Embolic stroke and cardiac papillary fibroelastoma. Clin Cardiol 2001; 24:346-7.

4)       Prasad A, Callahan MJ, Malouf JF. Acquired right atrial blood cyst: a hitherto unrecognized complication of cardiac operation. J Am Soc Echocardiogr 2003; 16: 377–378

5)       López-Pardo F, López-Haldón J, Granado-Sánchez C, Rodríguez- Puras MJ, Martínez-Martínez A. A heart inside the heart: blood cyst of mitral valve. Echocardiography 2008;25:928-30.

6)        

7)       Kuvin J, Saha P, Rastegar H, Salomon RN, Pandian N, Denofrio D. Blood cyst of the mitral valve apparatus in a woman with a history of orthotopic

8)       Dencker M, Jexmark T, Hansen F, Tydén P, Roijer A, Lührs C. Bileaflet blood cysts on the mitral valve in an adult. J Am Soc Echocardiogr 2009;22:1085.e5-8.

A complex case of PCI ( Rota-stenting strategy for heavily calcified coronary lesions ) ,

 A journal published article , written by Dr.Nabil Paktin