Sunday, November 27, 2016

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.


Friday, September 30, 2016

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.




Saturday, July 9, 2016

What is Electrical alternans vs. Pseudo-electrical alternans and pseudo literature reports ?

Electrical alternans is a broad term that describes alternate-beat variation in the direction, amplitude, and duration of any component of the ECG waveform (ie, P, PR, QRS, R-R, ST, T, U)
It was first recognized by Hearing in 1909 and further characterized by Sir Thomas Lewis in 1910 as occurring “either when the heart muscle is normal but the heart rate is very fast or when there is serious heart disease and the rate is normal.”
Kalter and Schwartz first identified electrical alternans on surface ECG in 1948
Electrical alternans must be distinguished from mechanical alternans (eg, pulsus alternans), although both may coexist 
The pathophysiologic mechanisms that cause electrical alternans can be divided into 3 categories:
-Repolarization alternans (ST, T, U alternans)
-Conduction and refractoriness alternans (P, PR, QRS alternans)
-Alternans due to cardiac motion


Electrical Alternans Associated with cardiac motion is due to alternation in the position of the heart with relation to recording electrodes.
The most common underlying disorder is an enlarged pericardial sac; however, not all pericardial effusions cause electrical alternans.
The presence of pericardial disease and total electrical alternans (P, QRS, and T wave) frequently suggests cardiac tamponade, but total electrical alternans is seen in only 5-10% of patients with cardiac tamponade.
Heart movement in patients with hypertrophic cardiomyopathy also may result in electrical alternans of this type .
Whenever what appears to be electrical alternans is not due to a large pericardial effusion, then pseudoelectrical alternans should be considered. Pseudoelectrical alternans is due to alternation in axis or amplitude because of events that alter conduction and do not alter the physical orientation of the heart.
In 1978, Klein, Segni and Kaplinsky coined the term ‘pseudoelec- trical alternans’ in a case report of intermittent left anterior hemiblock, in which the axis shifted every other beat due to the development of alternating normal and then leftward axis shift, presumably related to procaina- mide therapy.
Unfortunately, some literature defining interchangeably as true electrical alternans is a repolarization or conduction abnormality of the Purkinje fibers or myocardium.
Electrical alternans due to cardiac motion is effectively artifact, as the heart swings in relation to the chest wall and electrodes, with a period twice that of the heart rate. However, tamponade related electrical alternans is the true one .


Friday, July 8, 2016

Time course and hemodynamics of Mitral stenosis ( MS) causing Pulmonary arterial Hypertension ( PAH)

Mitral stenosis occurs
Left atrial pressure rise
Left atrium enlarges
Cephalization
PIE
PAH develops
PVR increases
RV enlarges
Pulmonic regurgitation develops
Tricuspid annulus dilates
Tricuspid insufficiency
RV failure


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