Abstract

I read the series1Thorne CD Hirshon JM Himes CD et al.Emergency medicine tools to manage smallpox (vaccinia) vaccination complications: clinical practice guideline and policy procedures.Ann Emerg Med. 2003; 42: 665-680Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar, 2Aragón TJ Fernyak SE The risks and benefits of pre-event smallpox vaccination: where you stand depends on where you sit.Ann Emerg Med. 2003; 42: 681-684Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar, 3Darling RG Waeckerle JF Grabenstein JD et al.Removing health care workers from clinical duties after smallpox vaccination: is it really necessary?.Ann Emerg Med. 2003; 42: 685-688Abstract Full Text Full Text PDF PubMed Scopus (2) Google Scholar on the smallpox vaccine in the November 2003 issue of Annals (articles #378, #418, and #419) with particular interest. I was one of the individuals who developed symptomatic coronary artery disease within 2 weeks of receiving the vaccine.I had none of the currently listed Centers for Disease Control and Prevention coronary artery disease exclusion risk factors for the vaccine. Although I'm an old guy, my exercise tolerance was unusually good before the vaccine. How many 52 year olds can clock 13 miles in 90 minutes with a sustained heart rate of 170 beats/min? On about the 10th day after receiving the vaccination, I experienced a new, intense retrosternal pain that dropped me to my knees. Like any good self-diagnosing emergency physician, I attributed it to a recent dietary change and esophageal spasm. I was getting ready to deploy with the Marines from Brooklyn, NY. By chance the day before, I acquired Nitrospray for anticipated use in this older reservist group of remarkable professionals. Not surprisingly, the discomfort was relieved by the spray. Ultimately, a coronary computed tomographic scan showed a single 80% lesion of the left anterior descending coronary artery without measurable arterial calcification. The lesion was confirmed at catheterization and stented.I am a former program director, and my residents have attested to my love of proposed pathophysiology of various disease states, which of course, changed from year to year. Nearly all individuals over 30 years old have some degree of coronary artery plaque formation that begins as fatty streaking in late adolescence. Macrophages interpolate themselves within the plaque and lie in wait to react with various antigenic stimuli.4Naruko T Ueda M Haze K et al.Neutrophil infiltration of culprit lesions in acute coronary syndromes.Circulation. 2002; 106: 2894-2900Crossref PubMed Scopus (543) Google Scholar, 5Neri Serneri GG Boddi M Modesti PA et al.Immunomediated and ischemia-independent inflammation of coronary microvessels in unstable angina.Circ Res. 2003; 27: 1359-1366Crossref Scopus (41) Google Scholar The seasonal variations in the frequency of symptomatic coronary artery disease are in part caused by the corresponding variations of viral and bacterial antigenic stimuli.6Pell JP Cobbe SM Seasonal variations in coronary heart disease.QJM. 1999; 92: 689-696Crossref PubMed Scopus (130) Google Scholar It is reasonable that the same strong vaccinia antigenic stimulus that causes encephalitis, myopericarditis, and Steven-Johnson syndrome can activate the macrophages, cascading the events of plaque rupture and clot formation.I know there is still some doubt about the linkage between the use of the vaccine and the development of symptomatic coronary artery disease,7Centers for Disease Control and Prevention Cardiac deaths after a mass smallpox vaccination campaign—New York City, 1947.MMWR Morb Mortal Wkly Rep. 2003; 52: 933-936PubMed Google Scholar possibly in part because individuals receiving the smallpox vaccine serve as their own control group. If 8 or 9 individuals developed symptomatic coronary artery disease within the first 3-week period after vaccine, one could expect a similar number from the cohort to develop symptomatic coronary artery disease in each of the subsequent 3-week periods. This did not happen. The clustering of coronary events within the 3-week time frame of vaccination supports a cause-and-effect relationship.Because of the live virus vaccine's known side effects, I initially had reservations about the benefit-to-risk ratio of vaccinating a large population against a disease whose last active case was more than 2 decades ago. However, I was confident that hard intelligence existed regarding the presence of smallpox and other weapons of mass destruction in Iraq.The smallpox vaccine has forever changed my life's perspective.In light of the current available data, it seems prudent to reassess the rationality of current policy and carefully reassess the risks and benefits of the vaccinia vaccination program. I read the series1Thorne CD Hirshon JM Himes CD et al.Emergency medicine tools to manage smallpox (vaccinia) vaccination complications: clinical practice guideline and policy procedures.Ann Emerg Med. 2003; 42: 665-680Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar, 2Aragón TJ Fernyak SE The risks and benefits of pre-event smallpox vaccination: where you stand depends on where you sit.Ann Emerg Med. 2003; 42: 681-684Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar, 3Darling RG Waeckerle JF Grabenstein JD et al.Removing health care workers from clinical duties after smallpox vaccination: is it really necessary?.Ann Emerg Med. 2003; 42: 685-688Abstract Full Text Full Text PDF PubMed Scopus (2) Google Scholar on the smallpox vaccine in the November 2003 issue of Annals (articles #378, #418, and #419) with particular interest. I was one of the individuals who developed symptomatic coronary artery disease within 2 weeks of receiving the vaccine. I had none of the currently listed Centers for Disease Control and Prevention coronary artery disease exclusion risk factors for the vaccine. Although I'm an old guy, my exercise tolerance was unusually good before the vaccine. How many 52 year olds can clock 13 miles in 90 minutes with a sustained heart rate of 170 beats/min? On about the 10th day after receiving the vaccination, I experienced a new, intense retrosternal pain that dropped me to my knees. Like any good self-diagnosing emergency physician, I attributed it to a recent dietary change and esophageal spasm. I was getting ready to deploy with the Marines from Brooklyn, NY. By chance the day before, I acquired Nitrospray for anticipated use in this older reservist group of remarkable professionals. Not surprisingly, the discomfort was relieved by the spray. Ultimately, a coronary computed tomographic scan showed a single 80% lesion of the left anterior descending coronary artery without measurable arterial calcification. The lesion was confirmed at catheterization and stented. I am a former program director, and my residents have attested to my love of proposed pathophysiology of various disease states, which of course, changed from year to year. Nearly all individuals over 30 years old have some degree of coronary artery plaque formation that begins as fatty streaking in late adolescence. Macrophages interpolate themselves within the plaque and lie in wait to react with various antigenic stimuli.4Naruko T Ueda M Haze K et al.Neutrophil infiltration of culprit lesions in acute coronary syndromes.Circulation. 2002; 106: 2894-2900Crossref PubMed Scopus (543) Google Scholar, 5Neri Serneri GG Boddi M Modesti PA et al.Immunomediated and ischemia-independent inflammation of coronary microvessels in unstable angina.Circ Res. 2003; 27: 1359-1366Crossref Scopus (41) Google Scholar The seasonal variations in the frequency of symptomatic coronary artery disease are in part caused by the corresponding variations of viral and bacterial antigenic stimuli.6Pell JP Cobbe SM Seasonal variations in coronary heart disease.QJM. 1999; 92: 689-696Crossref PubMed Scopus (130) Google Scholar It is reasonable that the same strong vaccinia antigenic stimulus that causes encephalitis, myopericarditis, and Steven-Johnson syndrome can activate the macrophages, cascading the events of plaque rupture and clot formation. I know there is still some doubt about the linkage between the use of the vaccine and the development of symptomatic coronary artery disease,7Centers for Disease Control and Prevention Cardiac deaths after a mass smallpox vaccination campaign—New York City, 1947.MMWR Morb Mortal Wkly Rep. 2003; 52: 933-936PubMed Google Scholar possibly in part because individuals receiving the smallpox vaccine serve as their own control group. If 8 or 9 individuals developed symptomatic coronary artery disease within the first 3-week period after vaccine, one could expect a similar number from the cohort to develop symptomatic coronary artery disease in each of the subsequent 3-week periods. This did not happen. The clustering of coronary events within the 3-week time frame of vaccination supports a cause-and-effect relationship. Because of the live virus vaccine's known side effects, I initially had reservations about the benefit-to-risk ratio of vaccinating a large population against a disease whose last active case was more than 2 decades ago. However, I was confident that hard intelligence existed regarding the presence of smallpox and other weapons of mass destruction in Iraq. The smallpox vaccine has forever changed my life's perspective. In light of the current available data, it seems prudent to reassess the rationality of current policy and carefully reassess the risks and benefits of the vaccinia vaccination program.

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