In patients with chronic obstructive pulmonary disease (COPD), cardiovascular comorbidities are highly prevalent and associated with considerable morbidity and mortality. This coincidence is increasingly seen in the context of a "cardiopulmonary continuum" rather than being simply attributed to shared risk factors, in particular, cigarette smoking. Both disease entities are centrally linked to systemic inflammation as well as aging, arterial stiffness, and several common biomarkers that led to the development of pulmonary hypertension, left ventricular diastolic dysfunction, atherosclerosis, and reduced physical activity and exercise capacity. For these reasons, COPD should be considered an independent factor of high cardiovascular risk, and efforts should be directed to early identification of cardiovascular disease (CVD) in COPD patients. Assessment of the overall cardiovascular risk is especially important in patients with severe exacerbation episodes, and the same therapeutic target levels for glycosylated hemoglobin, low-density lipoprotein cholesterol (LDL-C), or blood pressure than those recommended by clinical practice guidelines for patients at high cardiovascular risk, should be achieved. In this review, we will discuss the most recent evidence of the role of COPD as a critical cardiovascular risk factor and try to find new insights and potential prevention strategies for this disease.

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A 61-year-old man attended the emergency department with decreased level of consciousness, repetitive language, and memory loss. Clinical history included type II diabetes and hypertension. Domiciliary treatment included oral metformin 850 mg every 24 hours and oral indapamide 2.5 mg every 24 hours. Laboratory tests disclosed high glycemia (198 mg/dL), increased C-reactive protein (7.4 mg/dL), and normal renal function. Intravenous acyclovir of 800 mg every 8 hours was started on admission due to suspicion of viral encephalitis. Blood analysis on 10th day displayed hyponatremia (123 mmol/L) that was at first explained by the high water intake in the 3 preceding days; therefore, water restriction was decided. Nuclear magnetic resonance on day 14 identified an ictus and treatment with acyclovir was withdrawn. Three days after the withdrawal, plasmatic sodium levels began to increase (128 mmol/L) and returned to normal after 6 days (133 mmol/L). Although hyponatremia is not mentioned in the acyclovir summary of product characteristics, 2 reports in literature suggest that this drug could be a causative agent of hyponatremia. We believe that there is a relationship between acyclovir and hyponatremia. Application of the Karch and Lasagna algorithm to assess the causality of the reaction induced by acyclovir revealed the relationship to be possible.

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