In an adult post‑coronary artery bypass grafting patient with resting mean pulmonary artery pressure of 27 mm Hg that rises to approximately 33 mm Hg with minimal leg movement (heart rate 59 to 80 bpm), what are the recommended next diagnostic and therapeutic steps?

Management of Exercise-Induced Pulmonary Hypertension in a Post-CABG Patient

This patient has borderline resting pulmonary hypertension (mean PA pressure 27 mmHg) with exercise-induced elevation to 33 mmHg, requiring comprehensive evaluation to identify the underlying cause—most likely post-capillary PH from left heart disease given the CABG history—followed by treatment of the primary etiology rather than pulmonary vasodilators.

Hemodynamic Classification and Diagnostic Imperative

The resting mean PA pressure of 27 mmHg meets the diagnostic threshold for pulmonary hypertension (≥25 mmHg), and the 6 mmHg rise with minimal exercise suggests significant pulmonary vascular or left heart pathology. 1, 2

Critical Next Diagnostic Steps

Right heart catheterization with complete hemodynamic profiling is mandatory to determine whether this is pre-capillary or post-capillary PH, as this distinction fundamentally alters management. 1, 2 The catheterization must measure:

• Pulmonary artery wedge pressure (PAWP): If PAWP >15 mmHg, this indicates post-capillary PH from left heart disease (Group 2 PH). 1, 3
• Pulmonary vascular resistance (PVR): If PVR >3 Wood units with PAWP ≤15 mmHg, this defines pulmonary arterial hypertension requiring PAH-specific therapy. 1
• Diastolic pressure gradient (DPG): DPG ≥7 mmHg suggests combined pre- and post-capillary PH (Cpc-PH), indicating pulmonary vascular disease superimposed on left heart disease. 1
• Cardiac output: Essential for calculating PVR and assessing right ventricular function. 1

Most Likely Etiology: Post-Capillary PH from Left Heart Disease

In a post-CABG patient, Group 2 PH (pulmonary hypertension due to left heart disease) is by far the most common cause, present in 78.7% of PH cases in general cardiology populations. 1 Multiple clinical features strongly suggest this diagnosis:

High-Risk Features for PH-LHD in This Patient

• Prior CABG indicates established coronary artery disease and likely left ventricular dysfunction or diastolic dysfunction. 1
• Age and cardiovascular risk factors: Older patients with coronary disease commonly develop left heart failure with preserved or reduced ejection fraction. 1
• Exercise intolerance with minimal exertion: The inability to sustain even 30 seconds of minimal leg movement with heart rate rising only to 80 bpm suggests severe deconditioning or cardiac limitation. 1

Comprehensive echocardiography must specifically assess for:

• Left ventricular systolic and diastolic function (ejection fraction, E/e' ratio >14 suggests elevated filling pressures) 1
• Left atrial enlargement (>4.2 cm diameter) 1
• Valvular heart disease (mitral or aortic pathology) 1
• Right ventricular size and function 1
• Absence of mid-systolic notching in PA flow (its presence suggests pre-capillary PH) 1

Additional diagnostic workup should include:

• ECG: Look for left ventricular hypertrophy, left atrial abnormality, Q waves indicating prior MI, or atrial fibrillation. 1
• Chest imaging: Assess for Kerley B lines, pulmonary edema, or pleural effusions suggesting volume overload. 1
• BNP or NT-proBNP: Elevated levels support heart failure and correlate with prognosis. 4
• Pulmonary function tests and CT chest: Rule out Group 3 PH from lung disease (COPD, interstitial lung disease). 1, 5
• Ventilation-perfusion scan or CT pulmonary angiography: Exclude chronic thromboembolic PH (Group 4). 1, 5, 6

Treatment Algorithm Based on Hemodynamic Phenotype

If Post-Capillary PH (PAWP >15 mmHg) is Confirmed

Pulmonary vasodilators are contraindicated and potentially harmful in isolated post-capillary PH; treatment must target the underlying left heart disease. 1

Therapeutic priorities include:

1. Optimize heart failure management with guideline-directed medical therapy:

   • Diuretics (loop diuretics, thiazides, or aldosterone antagonists) to reduce volume overload and PAWP 1
   • ACE inhibitors/ARBs or ARNI for systolic dysfunction 1
   • Beta-blockers for rate control and cardioprotection 1
   • SGLT2 inhibitors for heart failure with reduced or preserved ejection fraction 1

2. Revascularization assessment: If angina or ischemia is present, consider stress imaging to evaluate graft patency and native vessel disease. 1

3. Valve intervention: If significant mitral or aortic valve disease is identified, surgical or percutaneous correction may reduce PA pressures. 1

4. Cardiac rehabilitation and supervised exercise training: Gradual reconditioning can improve functional capacity without worsening PH. 1

If Combined Pre- and Post-Capillary PH (Cpc-PH: PAWP >15 mmHg, DPG ≥7 mmHg, PVR ≥3 WU)

This phenotype indicates pulmonary vascular remodeling superimposed on left heart disease and carries worse prognosis. 1

Management approach:

• First, aggressively optimize left heart disease treatment as above. 1
• Referral to a pulmonary hypertension specialist is essential. 1, 4, 5
• PAH-specific therapy may be considered cautiously in expert centers, but evidence is limited and risk of pulmonary edema exists. 1

If Pre-Capillary PH (PAWP ≤15 mmHg, PVR >3 WU) is Confirmed

This would represent Group 1 (PAH), Group 3 (lung disease), Group 4 (CTEPH), or Group 5 PH, requiring subspecialist management. 1, 5

For Group 1 PAH:

• Acute vasoreactivity testing with IV epoprostenol, adenosine, or inhaled nitric oxide should be performed. 4
• If vasoreactive (≥10 mmHg fall in mean PA pressure to ≤40 mmHg with stable cardiac output), high-dose calcium channel blockers are first-line. 4
• If non-vasoreactive, initiate endothelin receptor antagonists (bosentan) or PDE-5 inhibitors (sildenafil, tadalafil). 4, 6
• Combination therapy is reasonable if monotherapy fails. 4

For Group 4 CTEPH:

• Pulmonary thromboendarterectomy is potentially curative and should be evaluated. 1, 6
• If inoperable, riociguat or balloon pulmonary angioplasty may be options. 1

Prognostic Considerations and Monitoring

Even mild PH (mean PA pressure 21-24 mmHg) is associated with increased mortality, and this patient's resting pressure of 27 mmHg with exercise elevation to 33 mmHg signals significant risk. 2, 7

The exaggerated exercise response (6 mmHg rise with minimal activity) suggests:

• Reduced pulmonary vascular compliance 1
• Impaired right ventricular-pulmonary artery coupling 1
• High risk for right heart failure progression 1, 8

Surveillance protocol should include:

• Clinical assessment every 3-6 months: NYHA functional class, 6-minute walk distance, symptoms 4
• Serial BNP/NT-proBNP measurements: Rising levels indicate worsening right heart strain 4
• Repeat echocardiography every 3-6 months: Monitor RV function, PA pressures, and left heart parameters 4
• Repeat right heart catheterization if clinical deterioration occurs or before therapy escalation 4

Critical Pitfalls to Avoid

Do not initiate pulmonary vasodilators empirically without hemodynamic confirmation of pre-capillary PH—this is Class III (harm) in post-capillary PH and can precipitate pulmonary edema. 4, 2

Do not rely on echocardiography alone for treatment decisions; right heart catheterization is mandatory before considering PAH-specific therapy. 4, 2, 7

Do not attribute dyspnea solely to deconditioning in a post-CABG patient with documented PH—underlying cardiac pathology must be thoroughly evaluated. 1

Do not use calcium channel blockers without documented acute vasoreactivity—they are ineffective and potentially harmful in non-vasoreactive PAH. 4

Multidisciplinary Care Model

This patient requires co-management by cardiology (for CABG follow-up and left heart optimization) and pulmonary hypertension specialists (if pre-capillary or combined PH is confirmed). 1, 4, 5 Management should occur at a center with expertise in both advanced heart failure and pulmonary vascular disease. 1, 4