Assessment of Silent Myocardial ischemia after primary PCI in anterior STEMI patients

INTRODUCTION

Silent myocardial ischemia (SMI) is the presence of objective evidence of ischemia without angina or equivalent symptoms. ¹

The objective evidence of SMI can be obtained from non-invasive diagnostic tests (exercise stress test, Holter-ECG, myocardial perfusion imaging, Echo-stress) or more recently by invasive tests during catheterization with the use of coronary pressure. ¹

Episodes of asymptomatic ischemia have been estimated to occur in a percentage ranging from 25% to 50% of the patients with ischemic heart disease and that this occurs, with respect to symptomatic episodes, with a ratio greater than 20:1. ² 

In silent myocardial ischemia (SMI), there are violations of perfusion, metabolism, function and electrical activity of the myocardium, which are not accompanied by clinical manifestations. ³

SMI can be an independent form of coronary heart disease or be combined with other forms of CHD. In the presence of SMI, the risk of sudden cardiac death increases 10 times, cardiac arrhythmias - 2 times, myocardial infarction and congestive heart failure - 1-1.5 times. ⁴

This study purposes to determine the incidence and to estimate the potential main causes of silent myocardial ischemia in anterior STEMI patient treated with PCI.

PATIENTS AND METHODS

This prospective cross sectional observational study included 50 patients from the attendants at Al Shiekh Zayed specialized hospital admitted with Anterior ST elevation myocardial infarction (STEMI) and received primary percutaneous intervention (1ry PCI) with complete revascularization of all lesions and have no residual coronary stenosis.

All patients included in this study were presented within 12 hours from symptoms onset and had an ECG showing persistent ST-segment elevation myocardial infarction precisely anterior STEMI and treated with primary PCI.

STEMI was defined as ST elevation at the J point, in at least 2 contiguous leads, ≥ 2 mm (0.2 mV) in men ≥ 40 years, 2.5 mm (0.25 mV) in men < 40 years or ≥1.5 mm (0.15 mV) in women in leads V2–V3 and/or ≥ 1 mm (0.1mV) in other contiguous chest leads or the limb leads.

Patients managed by any method other than primary PCI as thrombolysis or coronary artery bypass grafting (CABG) surgery were excluded. We also excluded Patients with residual -angiographically- significant coronary stenosis after 1ry PCI, Patients with symptoms suggestive of CAD or documented ischemia at follow up and Patients with ECG abnormalities that interfere with the diagnosis of ischemia include: ⁽¹⁸⁴⁾ Wolff-Parkinson-White pattern, Ventricular paced rhythm, Left Bundle Branch Block, Greater than 1 mm ST depression at rest and Left Ventricular Hypertrophy with ST-T abnormalities.

All enrolled patients were subjected to; medical history for diabetes mellitus and hypertension or if the patient currently on anti-diabetic and hypertensive medications. Family history of premature CAD, Smoking, Dyslipidemia, and Obesity.

Full assessment for general condition including; blood pressure, heart rate and rhythm, signs of pulmonary venous congestion. Additional heart sounds or murmurs. Lower limb edema, ascites, hepatomegaly and other signs of systemic venous congestion.

12 lead Electrocardiogram (ECG) was obtained at admission and follow up (1,3 and 6 months from discharge).

Laboratory investigationsincluded serum cardiac biomarkers (troponin I, creatine kinase and myocardial band of creatine kinase.Lipid profile: at discharge and follow up (3 and 6 months from discharge).

Transthoracic Echocardiography (TTE) was done for all included patientsbefore discharge and at follow up (1, 3 and 6 months after the event) using a Toshiba Ultrasound Machine according to the recommendations of American Society of Echocardiography to detect left ventricle size, left atrium size, left ventricular ejection fraction, any wall motion abnormalities or ischemic complicationssuch as (LV systolic dysfunction, LV aneurysm, LV thrombus, Secondary mitral valve regurgitation).

Coronary Angiography and Primary PCI within time window suggested by current guidelines (if symptoms of ischaemia are less than 12 hours duration and persistently elevated ST segment). Coronary artery Stenosis is mild if narrowing is less than 50%, moderate stenosis is between 50% and 70%, and severe or significant for a stenosis of 70% or more. Non-culprit stenosis was considered angio-graphically significant if they cause less than 70% luminal stenosis of the vessel on naked eye estimation. Complete revazcularization of significant stenosis in non-Infarction Related arteries was done for all patients with multi-vessel disease.

Treadmill Stress Test (TMT) was doneafter 6 months of the event according to Bruce Protocol provided that patients had no symptoms suggestive of myocardial ischemia and no new documented ischemic events.The interpretation of the exercise ECG focuses on the presence or absence of ischemic ECG changes along with any induced arrhythmias. TMT was considered "positive" for ischemia when there is ≥1 mm horizontal or downsloping ST segment depression in one or more leads that persists at 80 milliseconds after the J point. Depression of the J point (end of the QRS and beginning of the ST segment) is normally seen with increasing heart rates during exercise.it is probably related to atrial repolarization that extends through the QRS rather than myocardial ischemia. In this circumstance, the ST segment rapidly (within 80 milliseconds) returns to baseline. Patients were classified into 2 groups, (A) patients with TMT Positive, and (B) patients with TMT Negative.

RESULTS

Mean age was 54.54 ± 8.96 years. Men represented 78% (39 patients) of our study population while women represented 22% (11 patients). 44% (22 patients) were hypertensive while 40% (20 patients) were diabetic and 38% (19 patients) were smokers. From the 50 patients,14 patients (28%)

had a positive exercise treadmill test (TMT) at 6 months follow up and 36 patients (72%) were negative. All patients were completely asymptomatic during period of follow up. In patients with positive TMT, 3 patients (21.4%) were Smoker while in those with negative TMT, only 16 patient

(44.4%) weren’t Smokers which was statistically insignificant. (p value 0.132).  In patients with positive TMT, 3 patients (21.4%) were Obese while in those with negative TMT, only 10 patients (27.8%) weren’t Obese which was statistically insignificant. (p value p=0.734). In patients with positive TMT at follow up, zero patients (0%) had no Family history for CAD while in those with negative TMT, 7 patients (19.4%) had Family history for CAD which is statistically insignificant. (p value p=0.734) Figure (1). 

Fig. 1: the two studied groups were compared according to risk factors 

From the 14 patients with positive TMT, 11 patients were males (78.6%) and 3 females (21.4%). while in those 36 patients with negative TMT, 28 patients were males (77.8%) and 8 females (22.2%). but this difference was not significant statistically. (p= 1.000). In patients with positive TMT, mean age was (62.50 ± 4.01) years, while in those with negative TMT mean age was (51.44 ± 8.44) years which has statistical significance. (p value <0.001). Table (1). According to risk factors; In patients with positive TMT, 12 patients (85.7%) had DM while in those with negative TMT, only 8 patients (22.2%) had DM which has statistical significance. (p value <0.001). In patients with positive TMT at follow up, 8 patients (57.1%) were hypertensives while in those with negative TMT, only 14 patients (38.9%) weren’t hypertensives which was statistically insignificant. (p value 0.243). In patients with positive TMT at follow up, 13 patients (92.9 %) had Dyslipidemia while in those with negative TMT, only 14 patients (38.9%) were not dyslipidemics which has statistical significance. (p value <0.001) Table (2).  

Table 1: Comparison-between the included groups according to demographic data 

Table 2: the two studied groups were compared according to risk factors 

Table 3:  Comparison between the two studied groups according to resting TTE Echo

Table 4: Comparison between the two studied groups according to clinical examination:

Table 5:  Comparison between the two studied groups according to LAB results:

Table 6:  Comparison between the two studied groups according to PPCI.