Cardiac magnetic resonance (CMR) T1 mapping is a non-invasive method for determining the presence of myocardial fibrosis. T1 mapping determined myocardial fibrosis has been shown to be a prognostic marker of adverse cardiovascular events. In adult polycystic kidney disease (PCKD), cardiac remodelling is well established. Our aim is to determine whether PCKD patients may have increased myocardial fibrosis compared to controls.
PCKD patients were recruited from the nephrology clinics of a single centre. Volunteers without PCKD were recruited from the university staff, students as well as through advertisements. Non-contrast CMR examinations were performed with T1 and T2 mapping. Left ventricular (LV) and right ventricular (RV) contouring was performed by a single experienced operator. Univariate and multivariate linear regression were performed to determine the influence of multiple factors on the native T1 values.
83 PCKD patients and 40 volunteers (50% and 43.6% male respectively, p>0.05) were recruited. 5 patients were excluded for claustrophobia or suboptimal image quality. 1 volunteer was excluded for suboptimal image quality. Mean age of patients and volunteers is 40.2yrs±16.7yrs and 52.6yrs ±11.2yrs (p<0.001). Native T1 was significantly elevated in the PCKD patients compared to the volunteers (1266.2ms ±38.8ms vs 1236.6ms ±23.1ms respectively, p<0.0001). T2 values were not significantly different (59.2ms ± 6.1ms vs 56.9ms ± 5.8ms, p>0.05). Univariate linear regression demonstrated that PCKD, sex, age, body surface area, haemoglobin, urea, phosphate, hyperlipidaemia, ACE inhibitors and statins were statistically significant. Phosphate was excluded from modeling as phosphate results were not available for volunteers. On multivariable modeling, of only the statistically significant variables, only PCKD, sex and haemoglobin remained statistically significant and therefore were shown to be predictive independent variables of elevated native T1. Therefore, this indicates that PCKD patients have likely increased myocardial fibrosis as measured by T1 mapping compared to volunteers, adjusting for confounders.
Conclusion: PCKD patients have significantly elevated native T1 compared to volunteers which suggests increased myocardial fibrosis in PCKD patients. This association is independent of other significant confounders affecting native T1 values such as sex and T2 values. Further research is required to determine the long-term prognostic value of an elevated native T1 in PCKD patients and whether T1 mapping is modifiable.