HOCM 36%, congenital coronary arterial anomaly 17%, myocarditis 6%, RV arrhythmogenic cardiomyopathy 4%, i
Thursday, August 6, 2009
SUDDEN CARDIAC DEATH
The commonest causes are:
HOCM 36%, congenital coronary arterial anomaly 17%, myocarditis 6%, RV arrhythmogenic cardiomyopathy 4%, iron channel disorder 1%.So, that's 36% which are unaccounted for.
HOCM 36%, congenital coronary arterial anomaly 17%, myocarditis 6%, RV arrhythmogenic cardiomyopathy 4%, i
HOW TO LOSE WEIGHT
ATKINS DIET: High protein diets produce greater satiety and they increase thermogenesis, meaning that you burn off calories.
Wednesday, August 5, 2009
STROKE IN A PATIENT ON ASPIRIN
The MATCH study compared clopidogrel to clop-asp in the prevention of strokes for someone at a high risk of stroke. There was no statistically significant advantage of the combination, but it produced more bleeds. Therefore the right thing to do in someone who has had a stroke on aspirin is to change them to clopidogrel.
What about switching to clopidogrel?
It doesn't work for anyone except those with PVD - this was the result from CAPRIE where the only group that benefitted were those with PVD.
What about if you have AF and can't take warfarin? Does the addition of clopidogrel to aspirin provide better protection?
Marginally - ACTIVE looked at this and found ~1% reduction in stroke/year but a 0.7% increase in major bleeds.
ACTIVE investigators. Effect of Clopidogrel added to Aspirin in patients with Atrial Fibrillation. NEJM 2009; 360:2066-2078
What about increasing the dose of aspirin?
Unfortunately, that doesn't work:
These well-executed trials showed that an aspirin dose of 283 mg/d is unlikely to be more than 5% better than 30 mg/d7 and that 1200 mg/d is unlikely to be more than 25% better than 300 mg/d6 for stroke prevention, with small nonsignificant trends favoring the lower doses. In short, the best existing clinical evidence supports the concept that 75 mg/d aspirin is effective for stroke prevention and that higher doses may offer no additional protection.
The cumulative weight of existing clinical evidence favors low-dose (75 mg/d) aspirin, as advocated by Patrono and Roth.4
For patients who experience an initial or recurrent TIA while taking aspirin ("aspirin failures"), there is no good evidence that altering the dose of aspirin instead of continuing the original dose will reduce the risk of subsequent stroke.41 Those who experience TIA or minor ischemic stroke while taking aspirin appear to have a particularly high risk for subsequent stroke. Most clinicians empirically replace aspirin with another antiplatelet agent in this circumstance. Although such an approach seems sensible, it is not evidence based.41 42 43
REFERENCES:
4. Patrono C, Roth GJ. Aspirin in ischemic cerebrovascular disease: how strong is the case for a different dosing regimen? Stroke. 1996;27:756-760.[Abstract/Free Full Text]
41. Dyken ML. Aspirin dose in secondary prevention of stroke. Cerebrovasc Dis.. 1998;8:361–362. Letter.
SO...WHAT TO DO WITH A PATIENT WHO HAS A STROKE ON ASPIRIN?
Well, there's only one thing to do and that's to switch to Asasantin.
The ESPRIT Study Group. Aspirin plus dipyridamole versus aspirin alone after cerebral ischaemia of arterial origin (ESPRIT): Randomized controlled trial. Lancet 2006 May 20; 367:1665-73.
What about switching to clopidogrel?
It doesn't work for anyone except those with PVD - this was the result from CAPRIE where the only group that benefitted were those with PVD.
What about if you have AF and can't take warfarin? Does the addition of clopidogrel to aspirin provide better protection?
Marginally - ACTIVE looked at this and found ~1% reduction in stroke/year but a 0.7% increase in major bleeds.
ACTIVE investigators. Effect of Clopidogrel added to Aspirin in patients with Atrial Fibrillation. NEJM 2009; 360:2066-2078
What about increasing the dose of aspirin?
Unfortunately, that doesn't work:
These well-executed trials showed that an aspirin dose of 283 mg/d is unlikely to be more than 5% better than 30 mg/d7 and that 1200 mg/d is unlikely to be more than 25% better than 300 mg/d6 for stroke prevention, with small nonsignificant trends favoring the lower doses. In short, the best existing clinical evidence supports the concept that 75 mg/d aspirin is effective for stroke prevention and that higher doses may offer no additional protection.
The cumulative weight of existing clinical evidence favors low-dose (75 mg/d) aspirin, as advocated by Patrono and Roth.4
For patients who experience an initial or recurrent TIA while taking aspirin ("aspirin failures"), there is no good evidence that altering the dose of aspirin instead of continuing the original dose will reduce the risk of subsequent stroke.41 Those who experience TIA or minor ischemic stroke while taking aspirin appear to have a particularly high risk for subsequent stroke. Most clinicians empirically replace aspirin with another antiplatelet agent in this circumstance. Although such an approach seems sensible, it is not evidence based.41 42 43
REFERENCES:
4. Patrono C, Roth GJ. Aspirin in ischemic cerebrovascular disease: how strong is the case for a different dosing regimen? Stroke. 1996;27:756-760.
6. UK-TIA Study Group. The United Kingdom Transient Ischemic Attack (UK-TIA) aspirin trial: final results. J Neurol Neurosurg Psychiatry. 1991;54:1044-1054.
41. Dyken ML. Aspirin dose in secondary prevention of stroke. Cerebrovasc Dis.. 1998;8:361–362. Letter.
42. Grotta JC, Norris JW, Kamm B. Prevention of stroke with ticlopidine: who benefits most? TASS Baseline and Angiographic Data Subgroup. Neurology. 1992;42:111–115.
SO...WHAT TO DO WITH A PATIENT WHO HAS A STROKE ON ASPIRIN?
Well, there's only one thing to do and that's to switch to Asasantin.
The ESPRIT Study Group. Aspirin plus dipyridamole versus aspirin alone after cerebral ischaemia of arterial origin (ESPRIT): Randomized controlled trial. Lancet 2006 May 20; 367:1665-73.
CLOPIDOGREL AND PPI'S
The only PPI that does not prevent the bioactivation of clopidogrel is Pantoprazole (Somac).
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