{"id":866,"date":"2015-02-16T08:05:52","date_gmt":"2015-02-16T08:05:52","guid":{"rendered":"http:\/\/biomedpharmajournal.org\/?p=866"},"modified":"2017-01-05T07:11:20","modified_gmt":"2017-01-05T07:11:20","slug":"risk-factor-in-patients-of-cerebrovascular-accident","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol2no2\/risk-factor-in-patients-of-cerebrovascular-accident\/","title":{"rendered":"Risk Factor in Patients of Cerebrovascular Accident"},"content":{"rendered":"

Introduction<\/strong><\/p>\n

Stroke is a syndrome characterized by acute onset of neurologic deficit that persists for at least 24 hours, reflects focal involvement of the CNS.\u00a0 Amongst the leading neurologic disorder stroke is the 3rd<\/sup> most cause of death, disability, and health-care expenditure.(6)<\/sup><\/p>\n

Strong correlations between plasma lipids concentrations & risk of stroke have never been clearly established.\u00a0 The present study attempts to associate this; specifically showing the derangement caused in TC, HDL-c, & RF in CVA patients & also the effect of stroke on this derangement (on the 1st<\/sup> day, i.e. of admission after an acute onset & on 7th<\/sup> day of stroke).\u00a0 The present study establishes the role of lipids as a factor in stroke risk.\u00a0 Chief role of cholesterol in pathologic processes is a factor in the genesis of atherosclerosis of vital arteries, causing cerebrovascular, coronary, & peripheral vascular disease.\u00a0 There is also an established inverse relationship between HDL-c concentrations & coronary heart diseases including strokes, which is consistent with the function of HDL in reverse cholesterol transport.\u00a0 Many studies have been done which aims at derangement of lipids in stroke patients but not sufficient data is available for establishing the relationship between derangement of lipid patterns, especially showing the effect of risk factor, in CVA patients & also on the effect of stroke on this significant derangement particularly on the 1st<\/sup> day of admission after an acute onset of the disease and on the 7th<\/sup> day of stroke.\u00a0 The present study attempts to do so.<\/p>\n

Materials and Methods<\/strong><\/p>\n

Clinical material:\u00a0 The present work on,\u00a0 \u201cRisk factor in patients of cerebrovascular accident\u201d, was done in the Department of Medical Biochemistry, Gandhi Medical College, in association with the Department of Medicine, Hamidia Hospital, Bhopal, Madhya Pradesh.\u00a0 The clinical material for the present study comprised of 25 patients of CVA (20 males & 05 females), which were randomly selected from the emergency wards of medicine department, & 25 healthy subjects (15 males & 10 females), during the year 2004-05.\u00a0 All were in the age group 30-55 years and 56 & above years.<\/p>\n

Inclusion criteria:\u00a0 Cerebrovascular accident (CVA), were included irrespective of etiology.<\/p>\n

Exclusion criteria:\u00a0 Patients suffering from diabetes, hypertension, myocardial infarction, & cases of unconsciousness with fever and vomiting.<\/p>\n

Methods:\u00a0 Biochemical parameters included serum TC, HDL-c, & RF [TC: HDL-c] that were estimated colorimetrically using appropriate wavelength filters. The 12-14 hr fasting samples (approximately 5 ml of whole blood) of patients were taken within 24 hrs of admission, i.e. on the 1st<\/sup> day and then again on the 7th<\/sup> day during the period of hospitalization.\u00a0 For invitro quantitative determination of activity of lipid fractions in serum following kit methods were implemented.\u00a0 Kits were manufactured by Sigma diagnostics (India) Pvt. Ltd., Baroda.\u00a0 The data were statistically analyzed using \u2018t-test\u2019.\u00a0 The methods employed are shown in table 4.<\/p>\n

Results and Discussion<\/strong><\/p>\n

Observations seen in both the control & morbid groups are:<\/strong><\/p>\n

Mean Values of Lipid Profile in Control Group (table 1)<\/strong><\/p>\n

TC was reported at a value of (max \u2013 min) 195 \u2013 136 mgs\/dL which was in accordance with average mean TC values by Gardner (1929) (4)<\/sup>. Mean HDL-c & RF (54.12 \u00b1 8.93 & 3.9: 1 \u00b1 0.529) values were in accordance with the study conducted by Kiran Hasija & Hardeep K Bagga (2005) (6)<\/sup>.<\/p>\n

Tables:<\/p>\n

Observations seen in both the control & morbid groups are<\/p>\n

Table 1: Mean Values \u00b1 SD of Lipids in Control Group:<\/strong><\/p>\n\n\n\n\n\n\n
Biochemical<\/strong><\/p>\n

Parameter<\/strong><\/td>\n

Range [Max-Min]<\/strong><\/p>\n

(mgs\/dL)<\/strong><\/td>\n

Mean \u00b1 SD<\/strong><\/td>\n<\/tr>\n
TC<\/td>\n195 \u2013 136<\/td>\n159.36 \u00b1 15.865<\/td>\n<\/tr>\n
HDL-c<\/td>\n74 \u2013 40<\/td>\n54.12 \u00b1 8.931<\/td>\n<\/tr>\n
RF [TC: HDL-c]<\/td>\n3.9: 1 \u2013\u00a0 2.1: 1<\/td>\n2.968 \u00b1 0.529<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n

Table 2: Mean Values \u00b1 SD in Morbid Group on the Day of Admission.<\/strong><\/p>\n\n\n\n\n\n\n
Biochemical<\/strong><\/p>\n

Parameter<\/strong><\/td>\n

Range [Max-Min]<\/strong><\/p>\n

(mgs\/dL)<\/strong><\/td>\n

Mean \u00b1 SD<\/strong><\/td>\n<\/tr>\n
TC<\/td>\n398 \u2013 143<\/td>\n190.24 \u00b1 52.24**<\/td>\n<\/tr>\n
HDL-c<\/td>\n88 \u2013 25<\/td>\n38.68 \u00b1 11.8*<\/td>\n<\/tr>\n
RF [TC: HDL-c]<\/td>\n6.3: 1 \u2013\u00a0 3.4: 1<\/td>\n4.996 \u00b1 0.752*<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

* p < 0.001 (highly significant); ** p < 0.01 (significant) on comparison of 1st<\/sup> day values with control group.<\/p>\n


\n<\/strong><\/p>\n

Table 3: Mean Values \u00b1 SD in Morbid Group on 7th<\/sup> Day of Admission <\/strong><\/p>\n\n\n\n\n\n\n
Biochemical<\/strong><\/p>\n

Parameter<\/strong><\/td>\n

Range [Max-Min]<\/strong><\/p>\n

(mgs\/dL<\/strong><\/p>\n

)<\/strong><\/td>\n

Mean \u00b1 SD<\/strong><\/td>\n<\/tr>\n
TC<\/td>\n278 \u2013 124<\/td>\n158.16 \u00b1 33.65**<\/td>\n<\/tr>\n
HDL-c<\/td>\n63 \u2013 22<\/td>\n35.68 \u00b1 7.93***<\/td>\n<\/tr>\n
RF [TC: HDL-c]<\/td>\n5.9: 1 \u2013\u00a0 3.4: 1<\/td>\n4.5 \u00b1 0.691*<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n

* p < 0.001 (highly significant); ** p < 0.02 (significant); *** p > 0.05 (insignificant) when 1st<\/sup> day values were compared with those of 7th<\/sup> day.<\/p>\n

Table 4:\u00a0 Methods employed.<\/strong><\/p>\n\n\n\n\n\n\n
Lipid Parameter<\/strong><\/td>\nMethod<\/strong><\/td>\nWavelength<\/strong><\/p>\n

(nms)<\/strong><\/td>\n

Formula<\/strong><\/td>\nNormal Value (mgs\/dL)<\/strong><\/td>\n<\/tr>\n
TC<\/td>\nEnzymatic (CHE, CHO, & POD)<\/td>\n505 (green)<\/td>\nA (T)<\/u> * 200<\/sub><\/p>\n

A (S)<\/p>\n

 <\/td>\n

130 \u2013 250<\/td>\n<\/tr>\n
HDL-c<\/td>\nPTA Precipitation<\/p>\n

& Enzymatic Method<\/td>\n

505 (green)<\/td>\nA (T)<\/u> * 100<\/sub><\/p>\n

A (S)<\/p>\n

 <\/td>\n

30 \u2013 70<\/p>\n[Males = 30 \u2013 63]\n[Females = 35 \u2013 75]<\/td>\n<\/tr>\n
RF<\/td>\n—<\/td>\n—<\/td>\nTC:HDL-c<\/td>\n< 4:1<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n

 <\/p>\n

Mean Values in Morbid Group on the Day of Admission (table 2):<\/strong><\/p>\n

On statistical analysis of the values of first day in morbid group versus the control group highly significant values were found for HDL-c & RF (p < 0.001), whereas for TC (p < 0.01) the t-value was found to be significant.<\/p>\n

A recent overview of 10 prospective studies of association between plasma cholesterol concentration > 5.7 mmol\/l and stroke risk found a pooled risk of 1.31 which was statistically significant {Quiziblash N, etal (1992)} (11)<\/sup>\u00a0 Lindenstrom, etal (1994) showed that the association between plasma cholesterol and risk of non-hemorrhagic event is not log linear; only relatively high cholesterol concentrations are associated with significantly increased risk.(3)<\/sup>\u00a0 Some studies found positive association with total stroke {Nubiola AR, etal (1981) (9)<\/sup>, ischemic stroke {Quiziblash N, etal (1991) (12)<\/sup>} which was in accordance with the present study (p < 0.01) when compared with control group.\u00a0 Highest level found in the present study was 280 mgs\/dL (demonstrated as borderline high, 200 to 400 mgs\/dL, according to Burtis, etal (2001).<\/p>\n

The predictive power of low HDL-c concentrations in serum for CAD, independently of other risk factors, has been well demonstrated in numerous epidemiological studies involving populations {Assmann & Schulte (1992)} (1)<\/sup>.<\/p>\n

The present study demonstrated mean HDL-c value of 38.68 \u00b1 11.8 (ranged from 88 \u2013 25 mgs\/dl) on admission.\u00a0 A highly significant variation was found between HDL-c & stroke (p < 0.001). \u00a0Giubilei F, etal (1990) demonstrated that the mean lowest HDL-c value was observed in stroke patients (5)<\/sup>.\u00a0 The only prospective study that reported a relation between HDL-c and stroke risk is the Framingham Study, in which HDL-c has non-significant protective effect in both men and women and on ischemic stroke in men.\u00a0\u00a0 According to William J Marshal ideal HDL-c > 1.0; borderline = 0.9 – 1.0; & abnormal < 0.9 (lowest range in the present study was 25 mgs\/dl [0.65 mmol\/l]).<\/p>\n

Mendez I, etal (1987) demonstrated a correspondingly higher ratio of TC: HDL-c (p < 0.01) that could be marginally correlated with the present study with mean 4.996 \u00b1 0.752 mgs\/dL (6.3 to 3.4) (p < 0.001).(8)<\/sup><\/p>\n

Mean Values in Morbid Group on 7th<\/sup> Day of Admission (table 3)<\/strong><\/p>\n

All the values showed a considerable decrease on the 7th<\/sup> day of stoke.\u00a0 The values of HDL-c & RF, though were found to be decreased on 7th<\/sup> day, but didn\u2019t show a very much compatible difference.\u00a0 A significant relationship was seen in values of TC (p < 0.02), highly significant relation for RF values (p < 0.001), & insignificant relationship was noted for HDL-c (p > 0.05) values, when statistical analysis was done between 1st<\/sup> day Vs 7th<\/sup> day.\u00a0 Therefore it is concluded that TC & RF tends to fall on 7th<\/sup> day whereas no significant conclusion can be drawn out for values of HDL-c.\u00a0 Hence it can be said that stroke causes particular derangement in values of lipids, which tends to decrease as severity of stroke decreases.<\/p>\n

Comparison of 1st<\/sup> Vs 7th<\/sup> day<\/strong><\/p>\n

The present study demonstrated a considerable decrease in values on 7th<\/sup> day as compared to 1st<\/sup> day.\u00a0 Mean TC value was lower on 7th<\/sup> day and was in accordance with study by Mendez I, etal (1987).\u00a0 According to him serum TC in cerebral infarction patients (50 \u2013 69 years) was lowest on 7th<\/sup> day; intermediate on 1st<\/sup> day, and highest at 3 months, whereas HDL-c changed a little; however, the present study demonstrated HDL-c (p > 0.05) to be insignificant.\u00a0 The 1st<\/sup> day mean fasting HDL-c of cerebral infarction patients was significantly lower in subjects aged 50 \u2013 59 years than in those aged 60 \u2013 69 years (23 \u00b1 3 Vs 42 \u00b1 5 mgs\/dl), and there was correspondingly higher ratio of TC:HDL-c (p < 0.01).\u00a0 The present study demonstrates RF to be highly significant (p < 0.001) on statistical analysis on 1st<\/sup> day Vs 7th<\/sup> day.<\/p>\n

Similarly, according to Aull S, etal (1996) TC levels of group B patients (levels determined within 49 \u2013 168 hours after an acute event) were significantly lower than group A levels (12 \u2013 48 hours) (2)<\/sup>.\u00a0 The present study demonstrated significant association for both TC (p< 0.02) when 1st<\/sup> day was statistically analyzed versus 7th<\/sup> day.<\/p>\n

V Hachinski, etal (1996) demonstrated that plasma TC (p = 0.003) was significantly higher among patients with thromboembotic strokes and TIAs than among control subjects.(13)<\/sup>\u00a0 This is in accordance with the present study (p < 0.02).\u00a0 Therefore, the study shows specific derangement in lipids (due to the effect of stoke) with all parameters found to be decreased on 7th<\/sup> day, which is in accordance with study by Aull S, etal (1996) & Mendez I, etal (1987), which demonstrated that lipids tend to temporarily fall after an acute stroke.\u00a0 The phenomenon is probably not strictly related to inadequate nutrition that might result from the conservative early management of dysphagia because the same phenomenon has been seen in patients with many acute neurologic conditions.<\/p>\n

Thus to conclude, in the followup study a significant relation was seen for TC (p < 0.02) when compared with values on 1st<\/sup> day of admission while a highly significant relation (p < 0.001) was seen for RF values.\u00a0 These variations could be the result of conservative treatment, the patients underwent for the proceeding seven days.\u00a0 However, no significant change (p > 0.05) was seen in values of HDL-c.<\/p>\n

Conclusions<\/strong><\/p>\n

All the values showed a considerable decrease on 7th<\/sup> day as stroke severity decreased.<\/p>\n

Therefore all lipid parameters were found to be proportionally linked with stroke severity.\u00a0 These variations could be the result of conservative treatment the patients underwent for the proceeding 7 days.\u00a0 Therefore, CVA\/stroke causes a significant derangement in lipids while comparing the 1st<\/sup> day Vs 7th<\/sup> day values (with increased values on 1st<\/sup> day & considerable decrease on 7th<\/sup> day).<\/p>\n

TC should be considered as a significant risk factor for CVA.\u00a0\u00a0 HDL-c values couldn\u2019t draw out any significant conclusion.\u00a0 Whereas highly significant relationship was seen with RF in followup correlated with improved condition of patients on 7th<\/sup> day.\u00a0 However a larger study with more population of similar clinical background is needed to be planned to establish the role of low HDL-c as a risk factor in stroke; also predicting the role of CVA in causing derangement in levels of lipids.<\/p>\n

References<\/strong><\/p>\n

    \n
  1. Assmann G., Schulte H., Amm. J. Cardiol., 70, 733-737 (1992).<\/li>\n
  2. Aull S., Lalouschek W., Schnider P., Sinzinger H., Uhl F., Zeiler K., Am. J. Med., 101(3), 291-8, (1996).<\/li>\n
  3. Lindenstrom, etal, BMJ, 309, 11-15, (1994).<\/li>\n
  4. Gardner J.A. & Gainsborough H., Biochem. Jr., 21, 130-140, (1929).<\/li>\n
  5. Giubilei F., D. Antona R., Antonini R., Lenzi G.L., etal, Acta. Neurol. Scand., 81(1), 84-6, (1990).<\/li>\n
  6. Kiran Hasija & Hardeep K Bagga, Ind. J. of Clin. Biochem., 20(1), 62, (2005).<\/li>\n
  7. Li S.C., Schoenberg B.S., Wang C, et al, Neurology, 35, 1708-13, (1985).<\/li>\n
  8. Mendez I., Hachinski V., and Wolf B., Neurol., 37(3), 507-11, (1987).<\/li>\n
  9. Nubiola A.R., Masana L., Masdeu S., Rubies-Prat J., Arch Neurol, 38, 468, (1981).<\/li>\n
  10. Oliver Michael F., Editorial BMJ, 320, 459-460, (2000).<\/li>\n
  11. Quiziblash N., Duffy S.W., Warlow C., Mann J., Cerebrovasc. Dis., 2, 127-36, (1992).<\/li>\n
  12. Quiziblash N., Josh L., Warlow C., Mann J., BMJ, 303, 605-9, (1991).<\/li>\n
  13. Hachinski, C. Graffagnino, M. Beaudry, G. Bernier, C. Buck, A. Donner, J.D. Spence, G. Doig, and B.M. Wolfe, Archives of Neurology, 53(4), (1996).<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"

    Introduction Stroke is a syndrome characterized by acute onset of […]<\/p>\n","protected":false},"author":2,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[7],"tags":[],"class_list":["post-866","post","type-post","status-publish","format-standard","hentry","category-vol2no2"],"_links":{"self":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/866","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/comments?post=866"}],"version-history":[{"count":4,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/866\/revisions"}],"predecessor-version":[{"id":13169,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/866\/revisions\/13169"}],"wp:attachment":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/media?parent=866"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/categories?post=866"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/tags?post=866"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}