Background: Pulmonary hypertension (PH) is a disease condition leading to right‐sided cardiac hypertrophy and, eventually, right‐sided heart failure. Cardiac troponin I (cTnI) is a circulating biomarker of cardiac damage.

Hypothesis: Myocardial damage can occur in dogs with precapillary and postcapillary PH.

Animals: One hundred and thirty‐three dogs were examined: 26 healthy controls, 42 dogs with mitral valve disease (MVD) without PH, 48 dogs with pulmonary hypertension associated with mitral valve disease (PH‐MVD), and 17 dogs with precapillary PH.

Methods: Prospective, observational study. Serum cTnI concentration was measured with a commercially available immunoassay and results were compared between groups.

Results: Median cTnI was 0.10 ng/mL (range 0.10–0.17 ng/mL) in healthy dogs. Compared with the healthy population, median serum cTnI concentration was increased in dogs with precapillary PH (0.25 ng/mL; range 0.10–1.9 ng/mL; P < .001) and in dogs with PH‐MVD (0.21 ng/mL; range 0.10–2.10 ng/mL; P < .001). Median serum cTnI concentration of dogs with MVD (0.12 ng/mL; range 0.10–1.00 ng/mL) was not significantly different compared with control group and dogs with PH‐MVD. In dogs with MVD and PH‐MVD, only the subgroup with decompensated PH‐MVD had significantly higher cTnI concentration compared with dogs with compensated MVD and PH‐MVD. Serum cTnI concentration showed significant modest positive correlations with the calculated pulmonary artery systolic pressure in dogs with PH and some echocardiographic indices in dogs with MVD and PH‐MVD.

Conclusions and Clinical Importance: Serum cTnI is high in dogs with either precapillary and postcapillary PH. Myocardial damage in dogs with postcapillary PH is likely the consequence of increased severity of MVD.