Recurrent Acute Decompensated Heart Failure in a 75-Year-Old Post-CABG Male with Severe Secondary Mitral Regurgitation and Ischemic Cardiomyopathy Planned for MitraClip Therapy

 Introduction

Secondary mitral regurgitation is a frequent consequence of ischemic cardiomyopathy and adverse left ventricular remodeling. Progressive mitral regurgitation increases left ventricular volume overload, worsens heart failure symptoms, and contributes to recurrent hospitalizations. Patients with prior coronary artery bypass grafting (CABG), advanced left ventricular dysfunction, chronic kidney disease, and multiple comorbidities often carry prohibitive surgical risk, making transcatheter edge-to-edge repair (MitraClip) an attractive therapeutic option.

Case Presentation

A 75-year-old male, known case of coronary artery disease status post CABG, hypertension, type 2 diabetes mellitus, hypothyroidism, chronic kidney disease, and ischemic cardiomyopathy, presented with worsening shortness of breath corresponding to NYHA Class IV functional status.

He had experienced multiple recent admissions for decompensated heart failure. Prior to the current hospitalization, he had persistent symptoms despite guideline-directed medical therapy and had progressively reduced exercise tolerance. There was no documented history suggestive of an acute coronary syndrome during the present admission.

On arrival, he was in acute decompensated heart failure with severe dyspnea and tachypnea requiring intensive monitoring and aggressive medical stabilization. Respiratory distress necessitated non-invasive ventilatory support.

Past Cardiac History

The patient was a known case of multivessel coronary artery disease and had previously undergone coronary artery bypass graft surgery. Available records documented grafts to the LAD, diagonal, obtuse marginal and posterior descending/posterolateral coronary territories.

Following CABG, he developed ischemic cardiomyopathy with progressive left ventricular dysfunction and recurrent heart failure admissions.

Clinical Examination

At admission, the patient was clinically ill with features consistent with acute decompensated heart failure.

The dominant clinical problem was severe breathlessness with pulmonary congestion requiring NIV support. Repeated progress notes documented ongoing hemodynamic and respiratory instability requiring stabilization before consideration of definitive intervention.

Investigations

Hematological Parameters

  • Hemoglobin: approximately 8.9–10.3 g/dL
  • Total leukocyte count: 8,700–14,400/mm³
  • Platelet count: 1.35–2.02 lakh/mm³

Renal Function

The patient had underlying chronic kidney disease with superimposed worsening renal function during decompensation.

  • Blood urea: 89–103 mg/dL
  • Serum creatinine:

    • Baseline approximately 1.9 mg/dL
    • Increased to 2.9 mg/dL during hospitalization
    • Subsequently improved to 2.4–2.6 mg/dL following treatment

Electrolytes

  • Sodium: 144–150 mEq/L
  • Potassium: 3.5–4.8 mEq/L

Cardiac Biomarkers

  • Troponin-I: 83 ng/L

Arterial Blood Gas Analysis

Serial ABG assessments demonstrated fluctuating oxygenation and acid-base status consistent with acute heart failure and respiratory distress requiring non-invasive ventilatory support.



ECG shows sinus tachycardia (~128/min), left atrial enlargement, left axis deviation, and complete left bundle branch block (QRS 148 ms) in a patient with chronic ischemic cardiomyopathy. No definite acute ischemic changes are identifiable because of underlying LBBB.


Echocardiographic Evaluation

Initial Echocardiography During Acute Decompensation

The initial echocardiographic assessment revealed:

  • Severe left ventricular systolic dysfunction
  • LVEF approximately 25%
  • Severe mitral regurgitation
  • Moderate tricuspid regurgitation
  • RVSP approximately 50 mmHg
  • Preserved right ventricular function

The patient was receiving intravenous dobutamine support at the time of assessment.

Subsequent Detailed Echocardiography

Repeat echocardiographic evaluation demonstrated:

  • Regional wall motion abnormalities with apicolateral hypokinesia
  • Moderate to severe LV systolic dysfunction
  • LVEF approximately 40%
  • Grade III left ventricular diastolic dysfunction (E/e′ ≈31)
  • Severe mitral regurgitation with jet area approximately 9.6 cm²
  • Dilated left atrium
  • Good right ventricular systolic function
  • TAPSE approximately 10 mm
  • Trivial tricuspid regurgitation
  • No left ventricular thrombus
  • No significant pulmonary valve pathology
  • Collapsible IVC measuring approximately 1.4 cm

Overall findings were consistent with ischemic cardiomyopathy with severe secondary mitral regurgitation contributing significantly to recurrent heart failure.


Pre Op TEE was done 

https://youtu.be/4KsZ0qNnBhQ


Hospital Course

The patient was managed as acute decompensated heart failure with severe LV dysfunction and severe mitral regurgitation.

Treatment included:

  • Continuous intravenous furosemide infusion
  • Intravenous dobutamine support
  • Non-invasive ventilation
  • Spironolactone
  • Dual antiplatelet therapy (aspirin and clopidogrel)
  • Statin therapy
  • Anticoagulation with heparin
  • Insulin therapy
  • Supportive treatment including electrolyte correction and renal optimization

During hospitalization, gradual clinical improvement was achieved with decongestion and stabilization of respiratory status. Renal function showed partial recovery from its peak deterioration.

Despite stabilization, the patient remained at high risk because of:

  • Recurrent heart failure admissions
  • Severe secondary mitral regurgitation
  • Significant left ventricular dysfunction
  • Prior CABG status
  • Chronic kidney disease
  • Requirement for inotropic support during decompensation

Heart-Team Evaluation

The patient was evaluated jointly by the cardiology and cardiothoracic teams.

Given:

  • Advanced age
  • Previous CABG
  • Recurrent admissions for heart failure
  • Severe symptomatic secondary mitral regurgitation
  • Significant LV dysfunction
  • Chronic kidney disease
  • Elevated operative risk

a repeat surgical intervention was considered high risk.

After multidisciplinary discussion and counselling of family members regarding the severity of illness and available treatment options, a transcatheter strategy was preferred.

The plan was:

  1. Optimization of heart failure status.
  2. Assessment of graft and coronary status with contrast minimization whenever feasible.
  3. Detailed transesophageal echocardiographic assessment for procedural suitability.
  4. Proceed with transcatheter edge-to-edge mitral valve repair (MitraClip) if anatomical criteria are met.

Final Diagnosis

  1. Recurrent acute decompensated heart failure.
  2. Ischemic cardiomyopathy.
  3. Coronary artery disease, status post CABG.
  4. Severe secondary (functional ischemic) mitral regurgitation.
  5. Severe left ventricular systolic dysfunction (LVEF 25–40%).
  6. Grade III left ventricular diastolic dysfunction.
  7. Pulmonary hypertension (RVSP approximately 50 mmHg).
  8. Chronic kidney disease with acute worsening during heart failure decompensation.
  9. Type 2 diabetes mellitus.
  10. Hypertension.
  11. Hypothyroidism.

Conclusion

This case illustrates the complex management of recurrent acute decompensated heart failure in a post-CABG patient with ischemic cardiomyopathy and severe secondary mitral regurgitation. Although initial stabilization was achieved with intensive medical therapy including diuretics, inotropic support and non-invasive ventilation, severe mitral regurgitation remained a major contributor to recurrent heart failure. Considering the patient’s prior cardiac surgery, ventricular dysfunction and comorbidities, the heart team elected to pursue evaluation for transcatheter edge-to-edge mitral valve repair (MitraClip) as a less invasive strategy to reduce mitral regurgitation and potentially decrease future heart failure hospitalizations.


Comments

Popular posts from this blog

46M with ascites and portal hypertension

20F severe headache, neckpains and vomitings.

Cutaneous Clues in Secondary Adrenal Insufficiency Associated with Mixed Connective Tissue Disease: A Case Report