# Assessment of Cardiovascular Disease in Autosomal Dominant Polycystic Kidney Disease
## 8 Magnetic Resonance Imaging  
Several studies reported the presence of LVH in patients affected by ADPKD. The prevalence ranges widely depending on age, gender, and hypertension, varying between 19 and 48% [16; 53]. In the general population, the gold standard for the assessment of LV mass (LVM) is cardiac magnetic resonance imaging (MRI), but the evaluation of LVH and LVM is mainly performed via echocardiography. Cardiac MR more accurately determines left ventricular dimensions and the LV mass, enhancing information about the pattern of hypertrophy and myocardial fibrosis. In ADPKD patients, MRI is not usually performed for the evaluation of LVM. One single study performed cardiac MRI for the assessment of LV mass and LVH, reporting significantly a lower prevalence value compared to echocardiographic studies [54]. Five hundred and forty-three hypertensive patients with GFR > 60 mL/min per 1.73 m\({}^{2}\) underwent the MR assessment of LVM before starting an intensive angiotensin blockade. The enrolled patients were younger than 50 years, with the satisfactory control of blood pressure and a high incidence of angiotensin-converting enzyme inhibitor (ACEi) administration. The prevalence of LVH was 0.93% using LVMI and 3.9% using non-indexed LV mass. The normal range of LVM via MR was lower than that reported via echocardiography, as described in previous studies comparing LVM indexes determined via cardiac MRI and echocardiography [54]. The indices of LVM were accounted for body size, reporting that LVMI demonstrated the strongest correlation in patients with ADPKD. Systolic blood pressure measured at office, serum creatinine, and urine albumin were directly associated with LVMI. Female gender was inversely associated, as expected, because of the relation between gender and body size. The authors suggest that aggressive blood pressure control and use of ACEi in patients with ADPKD was associated with decreased LVH. Left ventricular mass determined from cardiac MR appeared to be lower than that determined via M-mode echocardiography; the greater accuracy of MRI should account for this discrepancy and may lead to different management options for patients [54; 55; 56]. Some authors also used MRI in ADPKD to evaluate pericardial effusion and found larger pericardial effusion thickness in ADPKD subjects compared to a population control matched for age, gender, and GFR. [PERSON] et al. [55] used MRI, including ECG-gated cine MR of the aorta and heart, to evaluate pericardial effusion independently with three observers, measuring the maximum pericardial effusion thickness in diastole using electronic calipers. All MRI exams were obtained on a 1.5 T using a body array coil (Sigma HDXT, GEHealthcare, Waukesha, WI, USA, or Magnetom Aera, Siemens Healthineers, Erlangen, Germany). Patients with ADPKD and a mean eGFR of 67 mL/min/1.73 m\({}^{2}\) demonstrated a significantly higher prevalence of pericardial effusion > 5 mm compared to matched controlled patients (21% in ADPKD patients, vs. 3% in control population). The occurrence of pericardial effusion was independent of heart failure, rheumatologic disease, increased fluid intake, or thyroid dysfunction. Pericardial effusion thickness significantly correlated with gender and right and left pleural effusion and negatively correlated with age. The retrospective measurement of pericardial effusion thickness was similar in MRI and echocardiography when echocardiographic images were retrospectively analyzed, but only two out of eight effusions seen on MRI were reported on the initial echocardiography reading performed when blinded to MRI results. The evidence of pleural and pericardial effusion on MRI highlights the need for further investigations in these patients to explain the pathophysiology.