Cardiohepatic Syndrome: Large-Volume Ascites as the Presenting Feature of HFpEF

A 48-year-old man with hypertension, hyperlipidaemia, type 2 diabetes mellitus, and recently diagnosed HFpEF presented to the emergency department with progressive shortness of breath, bilateral lower extremity oedema to the knees, orthopnoea requiring three pillows, and severely reduced exercise tolerance — unable to walk more than one block before stopping. He had been hospitalised approximately one month earlier for decompensated diastolic heart failure. He denied chest pain, palpitations, fever, or abdominal pain, though abdominal swelling was subsequently identified on imaging.

Initial chest radiography showed no focal infiltrates. Arterial blood gas analysis revealed mixed hypoxaemic hypercapnic respiratory failure, prompting initiation of BiPAP, after which respiratory status improved. BNP was elevated on admission compared to the prior admission and continued to rise during hospitalisation, peaking above 3300 pg/mL — a clear BNP signal supporting decompensated heart failure, in contrast to cases where obesity and other factors suppress NP production.

Physical examination confirmed bilateral pulmonary crackles and lower extremity pitting oedema. The combination of AKI, hypervolaemic hyponatraemia, mildly elevated troponin (interpreted as demand ischaemia), and cholestatic liver injury profile — with predominant alkaline phosphatase and bilirubin elevation over transaminases — suggested the cardiohepatic syndrome pattern rather than intrinsic hepatobiliary disease. Viral hepatitis serologies were negative.

Transthoracic echocardiography showed preserved LVEF 55–60%, severe concentric LV hypertrophy, mildly elevated right ventricular systolic pressure (~35 mmHg), and a dilated inferior vena cava with reduced inspiratory collapse — findings indicative of elevated right-sided filling pressures. Left heart catheterisation was performed, revealing nonobstructive coronary artery disease (only 30% mid-LAD stenosis, iFR 0.97) but a markedly elevated LVEDP of 29 mmHg — the hemodynamic confirmation of severe diastolic dysfunction driving systemic venous congestion.

Abdominal imaging identified the full extent of systemic venous congestion: magnetic resonance cholangiopancreatography (MRCP) demonstrated hepatomegaly, large-volume ascites, and a right pleural effusion without biliary obstruction. CT of the abdomen and pelvis confirmed mild-to-moderate ascites with generalised mesenteric congestion.

Figure 1

Coronal MRCP Without Contrast — Large-Volume Ascites and Right Pleural Effusion

Coronal magnetic resonance cholangiopancreatography demonstrating large-volume ascites (arrow) and an associated right pleural effusion (arrowhead), consistent with systemic venous congestion from elevated right-sided cardiac filling pressures. No biliary obstruction or pancreatic mass was identified — a critical negative finding that redirects the diagnostic evaluation away from hepatobiliary disease toward a cardiac aetiology. The coexistence of ascites and pleural effusion without biliary pathology is a hallmark of cardiohepatic syndrome in the setting of HFpEF with elevated LVEDP.

Figure 2

Axial CT Abdomen and Pelvis — Moderate Ascites with Mesenteric Congestion

Axial CT without contrast demonstrating moderate abdominopelvic ascites (arrow) and diffuse mesenteric congestion (arrowhead). Mesenteric congestion — oedema and engorged lymphatics within the mesentery — is the CT correlate of elevated portal venous and systemic venous pressure transmitted to the bowel mesentery. It is reversible with decongestive therapy and should not be mistaken for mesenteric ischaemia or malignant infiltration. This finding, combined with the ascites and pleural effusion, defines the extracardiac manifestation syndrome of systemic venous congestion in advanced HFpEF.

Gastroenterology and interventional radiology were consulted for diagnostic paracentesis to measure the serum-ascites albumin gradient (SAAG) and confirm the cardiac mechanism. However, by the time ultrasound-guided evaluation was performed, aggressive diuresis had already reduced the ascites volume to a level insufficient for safe paracentesis — a positive treatment response that paradoxically prevented definitive biochemical confirmation.

Figure 3

Ultrasound Before Planned Paracentesis — Minimal Residual Perihepatic Fluid

Ultrasound performed immediately before the planned diagnostic paracentesis demonstrating a thin residual perihepatic fluid collection (arrow) — insufficient for safe fluid aspiration. The dramatic reduction in ascites volume within the 24–48 hours of aggressive IV furosemide therapy is itself diagnostically informative: cardiac ascites typically responds rapidly and substantially to diuretic decongestive therapy, whereas cirrhotic and malignant ascites tend to be more resistant. The complete clinical and biochemical response to decongestion, without paracentesis, provided sufficient evidence to attribute the ascites to the cardiohepatic mechanism.

The patient was treated with IV furosemide, empagliflozin, and spironolactone, with lisinopril, carvedilol, atorvastatin, and metolazone temporarily held during portions of the admission due to AKI, bradycardia, worsening hyponatraemia, and transaminitis. Hyponatraemia was managed with fluid restriction, sodium chloride supplementation, and Ure-Na therapy. Renal and hepatic abnormalities improved progressively with decongestion. The degree of concentric LV hypertrophy despite reportedly controlled hypertension raised concern for possible cardiac amyloidosis, and outpatient cardiac MRI was recommended.

Discussion

Congestive hepatopathy is the result of sustained passive hepatic venous congestion driven by elevated right atrial and systemic venous pressures — a consequence of prolonged elevation of left-sided filling pressures in HFpEF that eventually overloads the right heart and transmits backward into the systemic venous circulation. The resulting hepatic sinusoidal hypertension impairs hepatocellular oxygenation and bile flow, producing the characteristic laboratory pattern of this case: cholestatic predominance (high alkaline phosphatase and bilirubin) with comparatively modest transaminase elevation. This pattern differs from hypoxic hepatitis — "shock liver" — which produces a more dramatic transaminase spike. Hepatomegaly, gallbladder wall thickening (from pericholecystic oedema), and ascites complete the anatomic picture. The critical diagnostic anchor in this case was the LVEDP of 29 mmHg on left heart catheterisation — an objective hemodynamic proof that elevated filling pressure, transmitted through the pulmonary circuit to the right heart and then to systemic veins, was the mechanism driving the apparent hepatic and abdominal pathology.

Cardiac ascites is a clinically underappreciated manifestation of advanced heart failure that can dominate the presentation and misdirect the diagnostic evaluation toward gastroenterology and hepatology rather than cardiology. When ascitic fluid can be obtained, cardiac ascites is distinguished from cirrhotic ascites by a SAAG ≥1.1 g/dL with ascitic total protein >2.5 g/dL — cirrhotic ascites has the same high SAAG but a lower protein concentration because the cirrhotic liver fails to secrete adequate albumin into the ascitic fluid, whereas in cardiac ascites the hepatic synthetic function is largely intact. This distinction has immediate management implications: cardiac ascites is treated with aggressive decongestive therapy including loop diuretics and SGLT2 inhibitors, not with the salt restriction and aldosterone antagonist-dominant regimen used for cirrhotic ascites. In this case, the rapid, near-complete resolution of large-volume ascites with IV furosemide and empagliflozin within 24–48 hours — before paracentesis could be performed — provided de facto proof of the cardiac mechanism through treatment response alone.