Introduction:

Hypertension is a leading identifiable and reversible risk factor for myocardial infarction, heart failure, atrial fibrillation, aortic dissection, peripheral arterial disease, stroke, kidney failure, etc with thrombus being the culprit lesion. South Asian ethnicity predisposes to higher mortality and morbidity from cardiovascular disease than other ethnic groups and is estimated to cause 7.5 million deaths, which accounts for 57 million disability-adjusted life years (DALYs). Hypertension causes changes in platelets (shape, size, expression of P-selectin, and sensitivity to catecholamines,) However, the data on platelet aggregation is sparse, inconclusive, and has shown contradictory results in Asian Indians. Therefore, this study is designed to study the platelet aggregation in Indian hypertensives and to investigate if platelet aggregation is determined by the level of blood pressure.

Materials and methods:

The study was conducted at the tertiary health center in 50 primary hypertensives & compared with age & sex-matched healthy controls. After ethics approval from IRB, an informed and written consent was taken. All subjects completed a physical and cardiovascular system examination. Blood pressure recordings were done as per JNC-VIII Guidelines and were further divided into sub-groups as per the JNC-VIII classification. Platelet rich plasma was used to estimate aggregation using a Chronolog aggregometer based on the principle of light transmission. ADP (5 µM) & Epinephrine (2µM) were added to PRP to induce platelet aggregation. The normal value of platelet aggregation was compared between study subjects and controls using Independent t test and Mann-Whitney Test.

Results:

After comparing platelet aggregation to ADP and epinephrine in primary hypertensives and healthy controls, 28 cases had stage I and 22 had stage II hypertension. The mean platelet aggregation to ADP in normotensives and primary hypertensives was 31.32±6.64 and 73±10.07, respectively (p value<0.0001). Similarly, the mean platelet aggregation to Epinephrine in normotensives and primary hypertensives was 24.82±5.51and 50.94±12.19, respectively (p value<0.0001). (Fig 1) Furthermore, platelet aggregability was found to be significantly increased in primary hypertensives as compared to controls. Moreover, it was further raised in stage II hypertensives in comparison to stage I hypertensives.(Fig 2) CONCLUSIONS: This study is the largest prospective study conducted on plasma from hypertensives and implicates platelet aggregation as a the causative factor leading to cerebrovascular accidents, ischemic heart diseases in primary hypertensives. Hence, any anti-hypertensive drug which confers additional anti-platelet aggregation properties may benefit in the management of hypertension especially in the Indian population. However, further larger studies are recommended to verify the same.