The patient was stable on admission with bradycardia at 34 beats/min, afebrile, respiratory rate 18 breaths/min, and oxygen saturation 95% on room air. Thirty minutes later, she developed hemodynamic instability with blood pressure 88/61 mmHg without signs of cardiogenic shock. She then began to desaturate, with oxygen saturation 90% on room air, and had mild bilateral basal crackles.

An emergency 12-lead ECG (Figure 1) showed absence of atrial activity with a junctional escape rhythm at approximately 34 beats/min. There was ST-segment elevation of about 10 mm in the inferior leads (DII, DIII, aVF), 5 mm in lateral leads (V4 - V5), and 2 mm in V4, with reciprocal ST depression in DI, aVL, aVR, and V1 - V3.

Bedside transthoracic echocardiography showed segmental hypokinesia predominantly affecting the inferior and inferolateral walls, with a left ventricular ejection fraction of 51% and grade 1 diastolic dysfunction. Right ventricular function was preserved and there was no mechanical complication.

Laboratory investigations revealed elevated cardiac troponin I (0.66 ng/mL), normal serum electrolytes, and renal impairment (GFR: 29 mL/min). Inflammatory markers were elevated (CRP: 24 mg/L). Lipid profile showed hypercholesterolemia (LDL: 1.76 g/L). HbA1c was 6.5%, NT pro BNP: 788pg/ml, mildly elevated liver enzymes<2N, and normal Full blood count.

Figure 1.Emergency ECG showing 3^rd degree sino-atrial block with Junctional escape rhythm, an inferior and apico-lateral STEMI.

Initial management included; Oxygen therapy, with target SpO2 at 94%, dual antiplatelet therapy (aspirin 300 mg and clopidogrel 600 mg with maintenance dose at 100 and 75 mg respectively), anticoagulation with enoxaparin, 10,000 UI/12 hr S/C, high-dose statin therapy: atorvastatine 80 mg, proton pump inhibitor, pantoprazole, analgesia, and, atropine (administered at 1 mg per dose with a cumulative dose of 3 mg which proved ineffective), fibrinolysis with streptokinase (after administration of hydrocortisone 100 mg slow IV then Streptokinase 1.5 MUI diluted to 50 cc with Dextrose 5% given within 60 min) was performed after exclusion of contraindications.

After thrombolysis, clinical improvement was noted with stabilization of blood pressure (120/68 mmHg) and reduction in bradycardia.

Serial ECGs showed 2 hrs, 6 hrs and 36 hours after thrombolysis respectively showed.

An accelerated idioventricular rhythm at about 90 beats/min, a regression of about 70% of the ST segment elevation at the apico lateral territory, and of about 40% at the inferior leads (Figure 2).

Sino atrial bloc, insignificant ST elevation at the apico lateral territory without Q necrosis wave, regression of the ST segment elevation of about 70% at the inferior leads but with presence of pathological Q wave as well as regression of the ST depression in the anteroseptal, and upper lateral leads, isolated ventricular ectopic beats (Figure 3).

Regular Sinus bradycardia at about 50 bpm, Q waves at the inferior leads with repolarization disorders (Figure 4).

Figure 2.Two hours ECG post Fibrinolysis, showing an accelerated idioventricular rhythm at about 90 beats/min.

Figure 3. Persisting complete Sino-atrial block with significant regression of ST segment elevation.

Figure 4. Return to sinus rhythm with sinus bradycardia at 50 beats/min.

Subsequent ECGs showed great variations fluctuating from sinus rhythm to a sinoatrial bloc.

The patient was later referred with medical assistance on Oxygen, to the nearest available PCI center about 720 km away by flight.

A temporary pacing catheter was placed just before the PCI through the right femoral vein.

2.7.1. Procedure and Findings

Figure 5. Coronary images before (A) and after thrombolysis (B); A very large RCA with significant stenosis in its second segment (Blue arrow) and restoration of RCA flow after thrombolysis (red arrows); Temporary pacing visible (black arrows).

Left Femoral Approach

Coronary network: Very large Right dominant.

Right Coronary Artery (RCA): Significant stenosis of the RCA in its second segment with extensive thrombosis involving all RCA2 and RCA3 (Figure 5(a)).

Left Main Coronary Artery: Normal length, 3.5 mm caliber, giving rise to Left Anterior Descending (LAD) and Circumflex (Cx) arteries.

LAD: Rudimentary with myocardial bridging, no significant stenosis (Figure 6).

Circumflex: Mildly atheromatous without significant stenosis, small caliber.

The patient underwent thrombectomy/aspiration, retrieving multiple thrombi (Figure 7), restoring flow in RCA2 (Figure 5(b)) and RCA3. Tirofiban was administered with intracoronary bolus and IV relay 6 hours post-procedure.

2.7.2. Evolution and Follow-Up

In the Cardiology ICU, the patient’s general condition improved with good ambient air saturation and regression of ST elevation in all concerned leads. She equally developed an Atrial fibrillation with spontaneous return to sinus rhythm.

Figure 6. Hypoplastic LAD artery (blue arrow).

Figure 7. Multiple thrombi aspirated.

The outpatient treatment consisted of apixban 2.5 mg bid, clopidogrel 75 mg od, Rosuvastatine/Ezetimibe 20/10 mg 1 tab in the evening, Ramipril 1.25 mg od, Dapaglifozine 10 mg od, Pantoprazole 40 mg od.

Also, lifestyle changes was requested, and consultation with a Dieteticien with HbA1C control in 3 months, Nephrology follow-up (kidney function improved)

As therapeutic project, the patient was scheduled for control PCI one month later and eventually cardiac readaptation