Nocturia is a well-recognized, but poorly characterized, manifestation of cardiovascular disease. Multiple studies have reported associations between hypertension and the presence and severity of nocturnal voiding [1]. Hypertension is associated with multiple cardiac abnormalities which independently heighten the risk for adverse cardiovascular outcomes [2], including left ventricular hypertrophy (LVH), left atrial enlargement (LAE), and prolonged QTc interval (p-QTc), However, the association between nocturia and these specific cardiac abnormalities is not well understood. This study aims to explore potential associations between nocturia and LVH, LAE, and p-QTc on electrocardiography (ECG).

Retrospective analysis of self-reported nocturnal voiding frequencies from 153 patients evaluated at an inner-city academic cardiology practice. Patient-reported nocturnal voiding frequency was recorded in the medical record at the time of routine clinical encounter. A nocturia database was compiled with institutional review board approval via a waiver of informed consent for retrospective analysis.

ECGs concurrent with the clinical encounter were abstracted and evaluated according to current American Heart Association guidelines by a reviewer blinded to nocturia status. ECGs were assessed for the presence of LVH (using the Cornell and Sokolow-Lyon criteria), LAE (product of the amplitude and duration of the terminal negative component of the P wave in lead V1 measuring ≥1 mm by 1 mm or a total duration of the P wave ≥120 ms in the inferior leads), and p-QTc (≥460 ms in women and ≥450 ms in men). A nocturnal voiding frequency of ≥1 void was selected as the cutoff for nocturia because existing literature on nocturia and non-dipping hypertension suggests that the largest decline in nocturnal systolic blood pressure occurs between 0 and 1 nocturnal voids rather than at higher nocturnal voiding frequencies [3]. A power calculation was not performed due to the paucity of foundational literature on ECG correlates of nocturia.

Three different multiple logistic regression models were used to predict LVH, LAE, and p-QTc based on nocturia status: Model I adjusted for age; Model II adjusted for age, sex, and race; Model III adjusted for age, sex, race, body mass index (BMI), hypertension, diabetes mellitus, and diuretic utilization.

A total of 153 patients met the criteria for inclusion. The study sample was predominantly female (74%) and self-reported African-American race (90%), with a high prevalence of obesity (63%), hypertension (78%), diabetes mellitus (33%), and diuretic use (40%). Nocturia was present in 77% of study subjects, while LVH, LAE, and p-QTc were present in 44%, 41%, and 29% of study subjects, respectively. Bivariate analysis revealed significant associations between nocturia and older age, African-American race, obesity, hypertension, diuretic use, LVH, and LAE. No such trends were observed between nocturia and sex, diabetes mellitus, and p-QTc. 

On multivariate analysis, nocturia was predictive of LVH according to Model I (OR 3.20, [1.18-8.69], p=0.022), Model II (OR 3.17, [1.16-8.69], p=0.025), and Model III (OR 2.99, [1.02-8.75], p=0.046). Nocturia also predicted LAE according to Model I (OR 4.72, [1.56-14.30], p=0.006), Model II (OR 4.71, [1.54-14.37], p=0.006), and Model III (OR 4.24, [1.32-13.57], p=0.015). No significant associations were observed between nocturia and p-QTc according to Model I (OR 1.51, [0.56-4.10], p=4.10), Model II (OR 1.39, [0.51-3.81], p=0.517), or Model III (OR 1.19, [0.41-3.49], p=0.747).

Nocturia predicts LVH and LAE, and this finding persists even after controlling for several relevant comorbid conditions. LVH is associated with reduced left ventricular compliance (requiring higher filling pressures), whereas LAE reflects higher left ventricular preload, and both mechanisms likely predispose patients to sodium and water retention. Consistently, existing volume overload, particularly in conjunction with recumbency during sleep, would be expected to increase preload and cardiac output, lending to increased nocturnal urine production. The absence of a significant association between nocturia and p-QTc may be attributable to the association of p-QTc with multiple other factors, including electrolyte abnormalities, medications, and aging. The specific mechanisms underlying both the presence and absence of associations between nocturia and LVH, LAE, and p-QTc merit further study.

LVH and LAE were both independently associated with nocturia in the outpatient cardiology setting. Further investigation into nocturia as a potential marker of underlying cardiovascular disease is warranted.

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