Impact of an Influenza Pandemic on the Mortality of Congestive Heart Failure in Older Japanese: The 1998 Japanese Influenza Pandemic

To the Editor: It is well known that the mortality of influenza-associated disease increases during an influenza pandemic.1 After an influenza pandemic of late 1998 to early 1999 in Japan, excess mortality exceeded twice that of January 1998.2 There have been several reports on increased mortality in older people at the time of an influenza pandemic, and congestive heart failure (CHF) has been reported to be one of the most important causes of death. However, there have been few reports on the mortality and clinical features of CHF patients during a pandemic. In this study, we examined the characteristics of influenza pandemic–associated CHF in older people in the 1998 Japanese influenza pandemic. The clinical characteristics and prognosis of 236 consecutive CHF inpatients (mean age 74 ± 11 years; 112 males and 124 females), who had been admitted to our hospital between April 1996 and October 1999, were retrospectively investigated. We classified the CHF patients into the following three groups: (1) the pandemic-associated group (who were admitted between November 1, 1998 and March 31, 1999, during the influenza pandemic, n = 36), (2) the winter control group (who were admitted during the same winter periods of the 2 years before the 1998 Japanese pandemic of influenza, during November 1, 1996 to March 31, 1997 and during November 1, 1997 to March 31, 1998, n = 57), and (3) the nonwinter control group (who were admitted during the four consecutive nonwinter periods from April 1 to October 31 of 1996, 1997, 1998, and 1999, n = 143). Table 1 summarizes the characteristics of the three CHF groups. Mortality, particularly that of older patients (age 75 and older) was significantly higher (8.3 times) in the influenza pandemic-associated group than in either of the control groups (both P < .03). The occurrence of severe CHF (requiring intubation or resulting in death) was also significantly higher (2.0 times) in the influenza pandemic–associated group than in the nonwinter group (P < .02). Risk factors or conditions that increase preload or afterload (renal failure, hypertension, and valvular disease) tended to be less common, but ischemic heart disease tended to be higher (P = .51, P = .08, respectively) in the influenza pandemic-associated group than the other control groups. There were no significant differences in the positive inflammatory findings (white blood cell> 9000mm3 or C-reactive protein> 2mg/dl) among the three groups. Our present findings indicate that the number of older patients with severe CHF and mortality in the older CHF patients increased during the influenza pandemic. Some cytokines have negative inotropic effects on the heart,3 and the plasma concentrations of cytokines are high in chronic heart failure.4 Although the prognosis of the CHF patients with inflammatory findings were similar to those without these findings, some cytokines induced by influenza infection might reduce cardiac function and exacerbate CHF, and increase the mortality of CHF, particularly in older patients. During an influenza pandemic, the prevention of influenza infection and more intense management for CHF should be stressed for the reduction of CHF mortality in older subjects.