54 M Acute Inferior Wall Myocardial Infarction Presenting as Acute Pulmonary Edema with Mobitz Type I AV Block in a Middle-Aged Diabetic Smoker Successfully Managed with Temporary Pacing and Culprit Vessel Revascularization

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 54M Acute Inferior Wall Myocardial Infarction Presenting as Acute Pulmonary Edema with Mobitz Type I AV Block in a Middle-Aged Diabetic Smoker Successfully Managed with Temporary Pacing and Culprit Vessel Revascularization


Dr. Deepthi mam (DM cardiology )

Dr. Ashwini mam ( DNB cardiology )

Abstract

Background: Inferior wall myocardial infarction (IWMI) may present with conduction disturbances and acute heart failure. Early recognition and prompt revascularization remain crucial for favorable outcomes.

Case Presentation: A 54-year-old male, known diabetic for 2 years, chronic smoker, and alcohol consumer, presented with progressive exertional dyspnea for 3–4 days that acutely worsened to severe breathlessness at rest on the morning of admission. The episode was associated with chest discomfort and diaphoresis. On presentation, he was tachypneic, hypotensive, hypoxemic, and had elevated jugular venous pressure with bilateral basal crepitations. Electrocardiography demonstrated inferior wall myocardial infarction with ventricular premature complexes in bigeminy and subsequently Mobitz type I second-degree atrioventricular block. Cardiac biomarkers were positive. Echocardiography revealed inferior basal regional wall motion abnormality, moderate left ventricular systolic dysfunction, mild right ventricular dysfunction, and a dilated inferior vena cava. The patient developed acute pulmonary edema (Killip class IV) and was managed with antiplatelet therapy, anticoagulation, diuretics, and supportive care. Coronary angiography demonstrated significant disease involving the left circumflex artery (LCX) and posterolateral ventricular branch (PLV). Percutaneous coronary intervention with drug-eluting stent implantation to the LCX and balloon angioplasty to the PLV was performed under temporary pacemaker support with restoration of TIMI III flow. The patient showed clinical improvement following revascularization.

Conclusion: Inferior wall myocardial infarction can present with acute pulmonary edema, ventricular ectopy, and atrioventricular conduction disturbances. Early coronary angiography and revascularization, along with appropriate hemodynamic stabilization, can result in successful outcomes even in high-risk presentations.

Keywords: Inferior wall myocardial infarction, Acute pulmonary edema, Mobitz I AV block, Left circumflex artery, Percutaneous coronary intervention, Temporary pacemaker.


Introduction

Acute inferior wall myocardial infarction (IWMI) accounts for approximately 30–40% of ST-elevation myocardial infarctions and may be associated with conduction abnormalities due to involvement of the atrioventricular nodal artery. Patients may present with varying degrees of heart failure ranging from mild congestion to cardiogenic pulmonary edema. The coexistence of acute pulmonary edema, ventricular arrhythmias, and atrioventricular block represents a high-risk clinical scenario requiring urgent stabilization and revascularization.

We report a case of acute IWMI presenting with severe pulmonary edema, ventricular bigeminy, and Mobitz type I atrioventricular block that was successfully managed with temporary pacing and percutaneous coronary intervention (PCI).


Case Presentation

Patient Information

A 54-year-old male presented to the emergency department on 09 June 2026 with complaints of:

  • Shortness of breath on exertion for 3–4 days.
  • Progressive worsening of dyspnea.
  • Sudden deterioration to severe breathlessness at rest on the morning of admission.
  • Associated chest discomfort.
  • Profuse sweating.

Past medical history was significant for:

  • Type 2 diabetes mellitus for 2 years.
  • Chronic smoking.
  • Chronic alcohol consumption.

There was no documented prior history of ischemic heart disease.


Clinical Course and Chronology

Three to Four Days Before Admission

The patient initially developed exertional breathlessness corresponding approximately to NYHA Class II–III symptoms. Over the next few days, symptoms progressively worsened.

Night Before Admission

He experienced increasing shortness of breath associated with chest discomfort and sweating.

Day of Admission

On the morning of admission, the patient developed severe breathlessness at rest (NYHA Class IV), prompting emergency medical evaluation.


Physical Examination

On arrival, the patient appeared distressed and tachypneic.

Vital Signs

  • Heart rate: 98–110 beats/min
  • Blood pressure: 90/60 mmHg
  • Respiratory rate: 34 breaths/min
  • Oxygen saturation: 79% on room air
  • Oxygen saturation improved to 96% with NIV oxygen support

Cardiovascular Examination

  • Elevated jugular venous pressure
  • Normal first and second heart sounds

Respiratory Examination

  • Bilateral basal crepitations

These findings were suggestive of acute congestive heart failure with pulmonary edema.


Initial Investigations

Electrocardiography

Initial ECG demonstrated:

  • Features suggestive of acute inferior wall myocardial infarction.
  • Ventricular premature complexes (VPCs).
  • Ventricular bigeminy.


Subsequent ECG revealed: ( after 1-2 hours )

  • Type I second-degree atrioventricular block (Mobitz I/Wenckebach).



Cardiac Biomarkers

  • Troponin-I: Positive ( 9420 )


Transthoracic Echocardiography

Two-dimensional echocardiography demonstrated:

  • Inferior basal left ventricular regional wall motion abnormality.
  • Moderate left ventricular systolic dysfunction.
  • Mild right ventricular systolic dysfunction.
  • Trivial tricuspid regurgitation.
  • Dilated inferior vena cava with reduced collapsibility, suggesting elevated right atrial pressure.


Clinical Diagnosis

Based on the clinical presentation and investigations, a diagnosis was made of:

Acute Coronary Syndrome

  • Acute Inferior Wall Myocardial Infarction

Complicated by:

  • Acute pulmonary edema
  • Moderate LV systolic dysfunction
  • Ventricular bigeminy
  • Mobitz type I AV block
  • Killip Class IV heart failure


Initial Management

The patient was admitted to the intensive cardiac care unit and initiated on:

Antiplatelet Therapy

  • Aspirin 325 mg loading dose followed by maintenance therapy.
  • Ticagrelor 180 mg loading dose followed by maintenance therapy.

Lipid-Lowering Therapy

  • Atorvastatin 80 mg loading dose followed by maintenance therapy.

Anticoagulation

  • Intravenous unfractionated heparin.

Heart Failure Management

  • Intravenous furosemide infusion.
  • Oxygen supplementation via non-rebreathing mask.

Additional Medications

  • Spironolactone 25 mg daily.
  • Pantoprazole prophylaxis.

The patient was stabilized with plans for early coronary angiography.


Coronary Angiography and Intervention

Following stabilization, coronary angiography was performed through the right femoral arterial approach.

Angiographic Findings

Coronary angiography revealed:

  • Significant disease involving the left circumflex artery (LCX).
  • Significant disease involving the posterolateral ventricular branch (PLV).

Given the associated atrioventricular conduction abnormality, a temporary transvenous pacemaker was inserted prior to intervention.


Percutaneous Coronary Intervention

PLV Intervention

  • Plain old balloon angioplasty (POBA) performed.
  • 2.0 × 12 mm balloon inflated up to 6 atmospheres.
  • Final TIMI III flow achieved.

LCX Intervention

  • Predilatation using a 2.5 × 12 mm balloon at 10 atmospheres.
  • Implantation of a 3.5 × 32 mm sirolimus-eluting drug-eluting stent.
  • Post-dilatation using a 3.5 × 8 mm balloon at 12 atmospheres.
  • Final TIMI III flow achieved.

The procedure was uneventful with excellent angiographic results.


Outcome and Follow-Up

Following successful revascularization:

  • Dyspnea improved significantly.
  • Pulmonary congestion resolved.
  • Hemodynamic parameters stabilized.
  • Coronary flow was restored with TIMI III perfusion.
  • Temporary pacing support was successfully utilized during the peri-procedural period.

Post procedure ECG 




The patient remained clinically stable after intervention and was continued on guideline-directed secondary prevention therapy.


Discussion

This case illustrates several important clinical aspects of inferior wall myocardial infarction:

1. Atypical Presentation

The predominant symptom at presentation was progressive dyspnea rather than classical prolonged chest pain. Diabetic patients frequently exhibit atypical manifestations of acute coronary syndromes.

2. Acute Heart Failure Presentation

The patient presented in Killip class IV heart failure with severe pulmonary edema, hypoxemia, elevated JVP, and pulmonary crepitations. Such presentations are associated with significantly increased mortality and warrant urgent reperfusion.

3. Conduction Abnormalities

Mobitz type I AV block is commonly associated with inferior myocardial infarction because the AV nodal artery usually arises from the dominant coronary circulation supplying the inferior wall. These blocks are often transient and improve following reperfusion.

4. Ventricular Arrhythmias

Frequent ventricular premature complexes and ventricular bigeminy likely reflected ongoing ischemia and myocardial electrical instability.

5. Importance of Early Revascularization

Prompt coronary angiography identified significant LCX and PLV disease. Successful PCI restored TIMI III flow and was associated with rapid clinical improvement.


Learning Points

  1. Acute myocardial infarction in diabetic patients may present predominantly as dyspnea rather than chest pain.
  2. Inferior wall myocardial infarction can be complicated by Mobitz type I AV block and ventricular ectopy.
  3. Acute pulmonary edema may be the presenting manifestation of myocardial infarction.
  4. Echocardiographic assessment is valuable for identifying regional wall motion abnormalities and ventricular dysfunction.
  5. Temporary pacing may be required in ischemia-related conduction disturbances during coronary intervention.
  6. Early revascularization with PCI remains the cornerstone of management and can result in excellent clinical recovery even in high-risk presentations.


Suggested Final Diagnosis

Acute Inferior Wall Myocardial Infarction (likely LCX territory) complicated by:

  • Acute pulmonary edema (Killip Class IV)
  • Moderate left ventricular systolic dysfunction
  • Mild right ventricular dysfunction
  • Ventricular bigeminy
  • Mobitz Type I second-degree AV block

Successfully treated with temporary transvenous pacing, PCI with DES to LCX, and POBA to PLV with final TIMI III flow restoration.


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