ABSTRACT
Background: Anaemia is common in patients admitted with acute myocardial infarction [AMI] and can badly affect the short and long term outcomes. Hospital acquired anaemia [HAA] is a type of anaemia which develops in patients during hospitalization with a normal haemoglobin level at the time of admission. There is very scant data regarding the causes for hospital acquired anaemia. This study was conducted in order to determine the causes and baseline characteristics of low haemoglobin level in AMI
Methods: This descriptive study was performed in Lady Reading Hospital Peshawar from 1[st] June 2013 to 31[st] May 2014. All the patients with AMI having normal baseline haemoglobin level at admission were included. Haemoglobin was rechecked on 5[th] day of admission to see whether patient develops HAA or not
Results: A total of 456 consecutive patients with AMI were screened for low haemoglobin. Low haemoglobin level [haemoglobin 70 years were 12 [14.3%]. hypertensives were 34 [40.5%], diabetics were 24 [28.6%], CKD was seen in 11 [13.1%], dyslipidemia in 17 [20.2%], and smokers were 16 [19%]. Upper GI bleed was found in 23 [27%], lower GI bleed in 7 [8.3%], hematuria in 6 [7.1%], possible coronary intervention in 7 [8.3%], and more than one cause in 14 [16.6%] patients, while no cause was found in 27 [32.14%] patients
Conclusion: One third of patients had no discernible cause of low haemoglobin, while one fourth of patients had isolated upper GI bleed as the main cause for hospital acquired low Hb
ABSTRACT
Our objective was to asses the effect of folic acid supplementation on homocysteine levels in patients with established coronary artery disease. This quasi experimental study was carried out at department of Cardiology, KRL Hospital, Islamabad during the period of May 2002 to December 2003. The patients with raised fasting homocysteine levels were supplemented with 5mg of folic acid and were followed up for a period of six months. The primary end point was the change in homocysteine level and secondary end point was untoward cardiac events. In primary end point, folic acid supplementations decreased mean plasma homocysteine concentration in 17 [56.7%] of the patients with mean change in homocysteine concentration of up to 7.7 +/- 9.3 micro mol/l. There was evidence of substantial interindividual variation in the homocysteine response including an increase in homocysteine in 13 [43.3%] subjects [mean increase 5.5 +/- 10.7 pmol/l]. In secondary end point, three patients were admitted with exacerbation of chronic stable angina; they were ruled out for any myocardial damage. Twenty seven patients had uneventful follow up. The variability of response to folic acid replacement with paradoxical rise in homocysteine levels in certain individuals mandate that we retest the homocysteine level in patients undergoing folic acid replacement to establish its continued salutary response