Semin Thromb Hemost 2010; 36(1): 049-058
DOI: 10.1055/s-0030-1248724
© Thieme Medical Publishers

Influenza and Cardiovascular Disease: Does Swine-Origin, 2009 H1N1 Flu Virus Represent a Risk Factor, an Acute Trigger, or Both?

Giuseppe Lippi1 , 3 , Massimo Franchini2 , 3 , Emmanuel J. Favaloro4
  • 1U.O. Diagnostica Ematochimica, Azienda Ospedaliero-Universitaria di Parma, Parma, Italy
  • 2Servizio di Immunoematologia e Medicina Trasfusionale, Azienda Ospedaliero-Universitaria di Parma, Parma, Italy
  • 3Dipartimento di Patologia e Medicina di Laboratorio, Azienda Ospedaliero-Universitaria di Parma, Parma, Italy
  • 4Department of Haematology, Institute of Clinical Pathology and Medical Research (ICPMR), Westmead Hospital, Westmead, Australia
Further Information

Publication History

Publication Date:
13 April 2010 (online)


Influenza infection has become an important focus of both public and medical attention because of high-level perceived clinical and public health effects, enormously amplified by the current and ongoing 2009 H1N1 flu pandemic, sustained by the swine-origin influenza A (H1N1) virus (S-OIV). The current transmission of this virus among humans appears much higher than that traditionally observed with seasonal influenza, raising several outbreaks of febrile respiratory infection ranging in severity from self-limited to severe, even life-threatening disease. Reliable biological and clinical evidence support a significant association between influenza infection and cardiovascular disorders, so that S-IOV might also be regarded as a potential multifaceted bioweapon able to affect the function of the cardiovascular system through a kaleidoscope of humoral, biological, and biochemical mechanisms. In acute coronary ischemic episodes, on one hand, it seems reasonable to consider any acute influenza virus infection as a precipitating factor that is the final event propelling predisposed individuals (e.g., those with preexisting coronary artery disease) over a threshold that precipitates the development of infarction in synergy with other well-known triggers. On the other hand, influenza virus-induced endothelial dysfunction, modification of lipoprotein metabolism, atherosclerotic plaque outgrowth, and inflammation additionally support the role of influenza infection as a strong cardiovascular risk factor. Comprehensive information regarding the 2009 H1N1 infection remains limited, so that it seems unreasonable to draw definitive conclusions. Nevertheless, current recorded mortality data would lead us to conclude that this new virus might represent a sinister threat to humankind, with cardiovascular mortality risk highlighting an additional crucial role for increasing further the alert against this threat. It also seems reasonable to support calls for vaccination against these viruses, both the seasonal and the new S-OIV, because this might represent a feasible strategy for short- and long-term prevention of virus-associated cardiovascular disease.


Prof. Giuseppe Lippi

U.O. Diagnostica Ematochimica, Azienda Ospedaliero-Universitaria di Parma

Strada Abbeveratoia 2/a, 43100 - Parma, Italy