SARS-CoV-2 Infection Doubles Mortality Risk in Hospitalized Heart Failure Patients

Patients admitted to the hospital with acute decompensated heart failure face a precarious clinical situation even under the best circumstances, and new research suggests that a concurrent SARS-CoV-2 infection makes that situation considerably worse. A retrospective cohort study conducted at a tertiary academic center in Germany examined more than 2,000 adults hospitalized with acute decompensated heart failure between March 2020 and December 2024, and found that those who also tested positive for the coronavirus died in the hospital at rates substantially higher than their uninfected counterparts. The findings, published in BMC Infectious Diseases, add to a growing body of evidence that viral respiratory infections can tip vulnerable cardiac patients into lethal territory.

The research team, led by investigators at Ruhr University Bochum’s Knappschaft Kliniken University Hospital, analyzed records from 2,002 adults treated for acute decompensated heart failure, a condition in which the heart suddenly cannot pump enough blood to meet the body’s demands, causing fluid buildup in the lungs and tissues. Among these patients, 246 individuals, or 12.3 percent, had laboratory-confirmed SARS-CoV-2 infection detected by reverse transcription quantitative polymerase chain reaction during their hospital stay. This molecular diagnostic technique amplifies and detects viral RNA, providing both a yes-or-no answer about infection and, through the cycle threshold value, an indirect gauge of how much virus a patient is carrying.

The raw numbers were stark. Patients with confirmed SARS-CoV-2 infection died in the hospital at a rate of 32.5 percent, compared with 20.6 percent among those without the infection. Intensive care unit admission was also more frequent in the infected group, at 61.4 percent versus 50.7 percent, and the need for invasive mechanical ventilation, in which a breathing tube and ventilator take over the work of the lungs, was nearly three times as common, affecting 6.5 percent of infected patients against 2.4 percent of uninfected ones. All of these differences reached statistical significance, with p values at or below 0.002.

Because raw comparisons between groups can be distorted by differences in age, comorbidities, and disease severity, the researchers applied multivariable regression models that adjusted for clinically relevant covariates. Even after this statistical correction, SARS-CoV-2 infection remained independently associated with in-hospital mortality, with an adjusted odds ratio of 2.63 and a p value of 0.0002. An adjusted odds ratio above 2 means that, holding other factors constant, infected patients had more than two and a half times the odds of dying during their hospitalization. The infection also remained independently linked to ICU admission, with an adjusted odds ratio of 1.79, and to invasive mechanical ventilation, with an adjusted odds ratio of 2.84.

The burden of infection extended beyond survival and organ support. Hospitalized heart failure patients who also carried SARS-CoV-2 spent significantly longer in the hospital and in the intensive care unit. After adjustment, infection was associated with an additional 9.23 days of hospital stay and an additional 7.85 days of ICU stay, both statistically robust findings. In a condition where timely decongestion and bed capacity are critical, such prolonged stays represent not only worse outcomes for individual patients but also meaningful strain on healthcare resources, particularly during periods when respiratory viruses circulate widely in the community.

One of the more technically interesting aspects of the study involved the use of cycle threshold values as surrogate markers of viral burden. In RT-qPCR testing, the cycle threshold, or Ct value, refers to the number of amplification cycles needed before viral RNA becomes detectable. Lower Ct values indicate that less amplification was required, which in turn suggests a higher concentration of virus in the sampled material. The researchers therefore reasoned that Ct values could serve as a rough proxy for how heavily infected each patient was at the time of testing.

Among the 246 infected patients, the analysis revealed that lower median Ct values were associated with higher in-hospital mortality, with an adjusted odds ratio of 0.89 per Ct unit and a p value of 0.0338. Because the odds ratio is below 1, each unit decrease in Ct value, corresponding to an increase in viral burden, was linked to greater odds of death. Lower minimum Ct values were also associated with longer hospital stays, with an adjusted beta of minus 0.44 days per Ct unit and a p value of 0.0359. Taken together, these findings suggest that patients with higher viral loads fared worse, raising the possibility that viral burden could help stratify mortality risk within this already vulnerable population.

The authors themselves urge caution in interpreting these viral load findings. Cycle threshold values are imperfect surrogate markers of viral burden because they depend on sampling technique, specimen type, timing of testing relative to infection onset, and the specific PCR assay used. A nasal swab taken poorly or late in the course of infection can yield a high Ct value even in a heavily infected patient. The researchers explicitly describe the Ct-based associations as hypothesis-generating and call for prospective validation in future studies before any clinical decision-making relies on viral load measurements in this setting.

Interestingly, the study found that the heart failure phenotype itself, meaning whether patients had reduced, mildly reduced, or preserved ejection fraction, and whether they were receiving guideline-directed medical therapy before admission, showed no consistent associations with major in-hospital outcomes. This suggests that the viral infection, rather than the specific characteristics of the underlying cardiac disease or its chronic treatment, was the dominant modifiable factor driving worse outcomes during hospitalization. In other words, the acute viral insult appeared to overwhelm the prognostic influence of chronic heart failure characteristics.

The clinical implications of this work are considerable. Acute decompensated heart failure patients represent a clinically vulnerable population in whom respiratory infections have long been recognized as dangerous triggers of decompensation. This study quantifies that danger in the specific context of SARS-CoV-2, showing that concomitant infection roughly doubles the adjusted odds of in-hospital death and dramatically extends length of stay. For clinicians, the findings argue for vigilant screening for SARS-CoV-2 in heart failure admissions during periods of viral circulation, for aggressive monitoring of infected patients, and for continued efforts at vaccination and infection prevention in this high-risk group. For researchers, the viral burden signal points toward a future where quantitative PCR results might do more than confirm infection, potentially helping to identify which heart failure patients need the most intensive care.

Subject of Research: Virology

Article Title: Impact of SARS-CoV-2 infection and viral burden on outcomes in acute decompensated heart failure

Article References: Nashtar, M. A., Sehovic, H., Salemdawod, M., Garipoglu, G., Ödemis, B., Tzalavras, A., Steinmetz, M., Canbay, A., Özçürümez, M., Varnavas, V., Patsalis, P. C., & Katsounas, A. (2026). Impact of SARS-CoV-2 infection and viral burden on outcomes in acute decompensated heart failure. BMC Infectious Diseases, 26(1), Article 1694. https://doi.org/10.1186/s12879-026-14407-y

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14407-y

Keywords: SARS-CoV-2, heart failure, COVID-19, viral load, in-hospital mortality, ICU admission, cycle threshold, acute decompensated heart failure, Impact, infection, viral, burden