In 2012, ischemic heart disease accounted for 7.4 million deaths worldwide. The age-standardized incidence varies among and within countries. The Global Registry of Acute Coronary Events (GRACE) study, which includes US patient populations, found that 38% of ACS patients have STEMI, whereas the second Euro Heart Survey on ACS (EHS- ACS-II) reported that around 47% of patients with ACS have STEMI. In industrialized countries the annual incidence of UA is in the region of 6 cases per 10,000 people. The incidence of ACS increases with age, with a higher incidence among men until the age of 70. Women who are 15 years postmenopausal are equally likely as men to develop ACS. Over 80% of patients who present with myocardial infarction report at least 1 of the major risk factors, including cigarette smoking, dyslipidaemia, hypertension, diabetes, and abdominal obesity.

The overall number of deaths from STEMI has declined steadily over the past 30 years, but it has stabilized over the past decade.^1,2 Both a decreased incidence of STEMI and a decline in the case fatality rate after STEMI have contributed to this trend^.3 According to estimates from the American Heart Association, the short-term mortality rate of patients with STEMI ranges from 5% to 6% during the initial hospitalization and from 7% to 18% at 1 year^.4 Mortality rates in clinical trial populations tend to be approximately half of those observed in registries of consecutive patients, most likely because of the exclusion of patients with more extensive comorbid medical conditions.

Although ischemic pre-conditioning has consistently proven to be cardioprotective, its clinical application is clearly limited. In hopes of making ischemic conditioning clinically relevant, Zhao et al^{. 5} used the principles of ischemic pre-conditioning but applied them after the ischemic event took place (closely mimicking the setting of an AMI) in a canine model of myocardial ischemia- reperfusion. Indeed, these brief episodes of coronary artery occlusion applied immediately after the ischemic insult limited the MI size in the same manners ischemic pre-conditioning.

Timely reperfusion salvages myocardium from tissue injury after prolonged ischemia. However, there is convincing evidence that sudden restoration of blood flow to ischemic myocardium may paradoxically exaggerate injury that is not present at the end of ischemia^(6,7,8). This reperfusion injury is primarily expressed as contractile and coronary vascular endothelial dysfunction, upregulation of adhesion molecules on the endothelium, and transendothelial emigration of inflammatory cells into the parenchyma, edema, infarction, and apoptosis ^(9,10,11). Modifying the hydrodynamic conditions (i.e., blood flow and intracoronary perfusion pressure) during the early period of reperfusion has been reported to reduce the extent of reperfusion injury in the ischemic region ^{(12,13,14,15)} For example, gradually increasing the perfusion rate and intracoronary pressure during the early minutes of reperfusion have been associated with a reduction in necrosis, attenuation in the release of CK and lactate dehydrogenase, and tissue edema ^(13,15,16). Therefore, mechanical manipulation of the early phase of reperfusion may reduce the extent of postischemic injury.

This case-control, cross sectional, hospital-based study was conducted at the SS Institute of Medical Sciences & Research centre, Davanagere, Karnataka. 50 cases and 50 controls have been taken in this study. Duration of study was from April 2016 to Oct 2017

Inclusion criteria:

• Male and female patients who were between 18 to
• Diagnosis of STEMI according to ACC/AHA ECG criteria and who are candidates for PCI.
• The culprit coronary artery had to be occluded at the time of admission (TIMI 0 flow grade), and had to be adequately reperfused (TIMI 2 to 3 flow grade) after

Exclusion criteria;

• Previous STEMI or non-STEMI within 6 months
• Patients in Killip class IV;
• Evidence of retrograde filling by collaterals at coronary
•  
• Severe multivessel coronary artery disease likely to require further interventions.
• Known severe abdominal aortic aneurysm (>50 mm); or severe peripheral artery disease (class III to IV).

Study tools & techniques:

Various epidemiological, clinical, hematological and biochemical parameters will be recorded in these patients,

Coronary Angioplasty:

All patients were premedicated with loading doses of Ecosprin (325 mg) and clopidogrel (600mg) and atorvastatin (80=mg) given to the patients. Coronary angiography was performed using a standard Seldinger technique. Iohexol (Omnipaque) was used as contrast agent for coronary angiography. Coronary angiography allowed identification of the culprit coronary artery and checked that reperfusion had not occurred before PTCA (TIMI 0 flow grade) and that no collateral filling from homolateral or contralateral coronary vessels was present.

After diagnostic angiography, eligible patients will be randomized 1:1 to PCI+ remote ischemic post conditioning or conventional primary PCI . All eligible patients will be prepared with a thigh-sized limb cuff before arterial puncture (contralateral in case of femoral access). In the active treatment group, the protocol will be started with thrombectomy. The lower limb will be exposed to 3 cycles of ischemia/reperfusion, each obtained by 5 min cuff inflation at 200mmHg, followed by 5 min complete deflation. End point of the study will be enzymatic infarct size assessed by the area under the curve of creatine kinase-myocardial band (CK-MB) release. In the end coronary angiography was performed in both groups to assess coronary patency and to estimate the myocardial perfusion index using the blush grade evaluation. The angioplasty procedure was then complete according to physician judgment with respect to patient status.

Standard 12-lead ECGs were recorded at admission and 48 hours later. Maximal ST-segment change was measured by a cardiologist unaware of the patient‘s group. At all time points, ST-segment shift was measured 80 ms after the J point.

Blood samples were taken at admission, after 4 hours of opening of the artery, then after 8 hours, 24 hours, 48 hours, 72 hours.

In the postconditioned group, the mean age was 64.90±6.27yrs. In the control group, the mean age was 57.80±8.79.The histogram for this population is depicted below.

Among cases 20 patients were male and 30 patients were female respectively. Among control group 35 patients were male and 15 patients were female respectively

In the postconditioned group, the mean BMI was 28.80±5.51.In the control group, the mean BMI was26.50±1.51.

Out of 50 patients in cases 20 patients (40%) were smokers and in the control group 20 patients (40%) were smokers.

Out of 20 patients in cases 20 patients (40%) were dyslipidaemic and in the control group 10 patients (20%)

PRESENCE OF DIABETES BETWEEN TWO GROUPS:

FREQUENCY      DISTRIBUTION OF          EJECTION FRACTION     IN STUDY POPULATION:

There is no statistically significant difference of between two groups. (P=0.69)

DISTRIBUTION OF CULPRIT VESSEL BETWEEN TWO GROUPS:

Among cases 15(30%) patients had LAD, 15(30%) patients had LCX and 20(40%) patients had RCA as their culprit vessel respectively. Among control group 30(60%) patients had LAD, 5(10%) patients had LCX and 15(30%) patients had RCA as their culprit vessel respectively.

BLUSH GRADING AFTER PRIMARY PCI BETWEEN TWO GROUPS:

Among cases 25 patients (50%) had blush grade 3, 10 patients (20%) had blush grade 3 and 15 patients (30%) had blush grade 1 respectively after primary PCI. Among control group 10 patients (20%) had blush grade 3, 20 patients (40%) had blush grade 2 and 20 patients (40%) had blush grade 1 respectively after primary PCI. There was no statistical significance between the two groups.

In the control group and post conditioned group, the mean age was 57.8 years +/- 8.79 years and 64.9 years +/- 6.27 years. There was no statistical difference between the two groups. ( p=0.007).

Among cases 20 patients (40%) were male and 30 patients (60%) were female respectively. Among control group 35 patients (70%) were male and 15 patients (30%) were female respectively. There was no statistically significant difference of sex distribution between two groups. (p=0.005). Thus, in a hospital-based study, women patients form a little less number comparably.

In the control group, the mean BMI was 26.50 years +/- 1.51 years. In the postconditioned group, the mean BMI was 28.80 years +/- 5.51 years. There was no statistically significant difference of BMI between two groups(p<0.05).

Thus, most of the patients in both case and control groups were overweight. Previous studies also support that obesity and overweight are risk factors for AMI17

Out of 50 patients in cases, 40 patients (80%) and in the control group 25 patients (50%) were hypertensive respectively. There was no statistically significant difference of between two groups. (p=0.003). Out of 50 patients in case group 20 patients (40%) and in the control group 10 patients (20%) were dyslipidaemic respectively. There was no statistically significant difference of between two groups (p=0.029). These high prevalence of hypertension and dyslipidaemia in the study group are in accordance with the risk factors of AMI.

Out of 50 patients in cases, 20 patients (40%) and in the control group 20 patients (40%) were smokers respectively. There was no statistically significant difference of between two groups (p=1.000). In Indian subcontinent percentage of smokers are quite high and this has been reflected in our data.

Out of 50 patients in cases 10 patients (20%) and in the control group 10 patients (20%) were diabetic. There is no statistically significant difference of between two groups (p=1.00). The prevalence of diabetes has increased in India in last two decades18 and high prevalence of diabetes in study group indicates its strong correlation with AMI.

There was no statistically significant difference of ejection fraction between case (47.80 +/- 5.027) and control (43.40+/- 5.175) groups (p=0.69). Among cases 15(30%) patients had LAD, 15(30%) patients had LCX and 20(40%) patients had RCA as their culprit vessel respectively. Among control group 30(60%) patients had LAD, 15(30%) patients had LCX and 5(10%) patients had RCA as their culprit vessel respectively. There was no statistically significant difference of between two groups (p<0.5).

Mean ST segment deviation at 0 hour between cases and control group were 4.2 +/- 1.088 mm and 4.3 +/- 0.789 mm respectively. There was no statistically significant difference of between two groups (p=0.092).

Among cases 28 patients (56%) had blush grade 3, 15 patients (30%) had blush grade 2 and 7 patients (14%) had blush grade 1 respectively after PCI

Among control group 10 patients (20%) had blush grade 3, 20 patients (40%) had blush grade 2 and 20 patients (40%) had blush grade 1 respectively after PCI. There was significant statistically significant difference of between two groups.

Abnormalities associated with increasing myocardial perfusion, as assessed by the myocardial blush grade (MBG) correlate with unfavorable ventricular remodeling and risk for mortality even after adjusting for the presence of TIMI grade 3 flow or a normal TIMI frame count.19, 20. They are better indicator for microvascular integrity. In this study short term or long-term clinical outcomes were not assessed, instead of that laboratory and cath lab markers were assessed for successful reperfusion and cardiac injury. Myocardial blush grading is one of the markers for successful reperfusion at microvascular level. In our study in the post conditioned group there was significant improvement of myocardial blush grading indicating favorable result with post conditioning. Though previous studies on post conditioning showed similar effect, recently a large study conducted by Joo-Yong Hahn didn ‘t not find any significant difference of MBG between post conditioned and control group.22. In their study postconditioning was not performed per protocol in around 10% of patients and balloon occlusion for ischemic postconditioning was performed before stenting so there may be a possibility of incomplete establishment of flow before postconditioning violating the basic principle of post conditioning. Moreover, they used predilatation balloon and thrombosuction catheter for establishment of flow in most of the patients. In our study we have used thrombosuction catheter in most of the patients. The reason behind that was by use of predilatation balloon we are actually allowing more thrombus to migrate towards distal microcirculation causing more damage to microcirculation which is against the principle of direct stenting which should be a preferred strategy for management of STEMI. We have used thrombosuction catheter in almost all patients for establishing flow. The reason behind this strategy was that most of the patients in the study group had initial TIMI 0 or 1 flow. Now before putting stents, we have to see the distal segments. Thrombosuction catheter has advantage over predilatation balloon that chances of distal thrombus migration is less in case of thrombosuction catheter. In our institution we use predilatation balloon for establishing flow as a bail out strategy. To this regard it was postulated that cardioprotective effects of postconditioning may also be attenuated by thrombus aspiration because thrombus aspiration was reported to improve myocardial reperfusion. 22 Remote ischemic post conditioning was also associated with improvement in myocardial blush grading (MBG). MBG has been proposed as a more efficient marker of successful microvascular reperfusion than TIMI flow grade and TIMI frame count and has been positively associated with long-term mortality 23 in STEMI patients.

Remote ischemic post conditioning was also associated with improvement in myocardial blush grading (MBG). MBG has been proposed as a more efficient marker, obtaining such a beneficial effect by simple manipulation of reperfusion is of major potential clinical interest. Obviously, it represents a feasible, safe, and efficient cardioprotective intervention. Additional studies are needed to address its effect on postischemic functional recovery, no reflow, and even cardiovascular morbidity within the months after AMI. Important research must be done to understand the molecular mechanism of this protection to develop new drugs to apply pharmacological postconditioning to all patients with AMI.

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