Transient Ischemic Attack Could Double Risk of MI

Individuals who have had a transient ischemic attack are twice more likely than are those in the general population to have a myocardial infarction, indicating that TIA might be a significant risk factor for MI, according to a population-based study that was published online in Stroke on March 24.

In addition, "in the population of patients with TIA we studied, having MI increased the risk of death by a factor of three. This supports the concept of careful primary prevention of CAD [coronary artery disease] in TIA patients, even in the absence of symptoms. It also suggests that screening for CAD in at least some TIA patients may be reasonable," wrote Dr. Joseph D. Burns and his coinvestigators at the Mayo Clinic in Rochester, Minn. (Stroke 2011;42 [doi: 10.1161/STROKEAHA.110.593723]).

The researchers studied a community-based cohort of patients with incident TIA that was identified retrospectively through the Rochester Epidemiology Project Medical Records Linkage System, which holds medical record data for these individuals for all care provided, as well as and autopsy or death certificate information.

The investigators identified a cohort of Rochester residents who had incident TIA during 1985-1994 and a cohort of Olmsted County (Minn.) residents who had incident MI during 1979-2006.

A total of 456 Rochester residents had an incident TIA in 1985-1994. Of these, 15% (68) had a history of MI before TIA and were excluded from the analysis. Therefore the study results pertain to the 388 remaining patients.

On average, patients were 71 years old at the time of TIA and 41% of the patients were male. In terms of cardiovascular risk factors, 62% had hypertension, 11% had diabetes mellitus, and 55% were current or former smokers. Based on TOAST (Trial of ORG 10172 in Acute Stroke Treatment) subtypes, 19% of the TIAs were attributable to large artery atherosclerosis, 13% were cardioembolic, 6% were lacunar, and 5% were attributable to other causes. Importantly, a single etiology could not be clearly established for 57% of the TIAs.

Median follow-up for patients who had a TIA was 10 years. Of these, 44 patients had an MI after the TIA – an average annual incidence of MI after TIA of 0.95%. Median time from index TIA to index MI was 4.6 years. The risk of MI after TIA remained essentially constant over time, based on a survival analysis.

The age-, sex-, and period-specific relative risk for incident MI in patients who had TIA – when compared with that of the general population – was 2.09. Interestingly, this elevated risk was most pronounced in TIA patients younger than 60 years old. For those younger than 60 years, that relative risk was 15.1, when compared with the general population. In comparison, for patients 60 years and older, the age-, sex-, and period-specific relative risk for MI aggregated over three age groups (60-69 years, 70-79 years, and 80 years or older) was 1.93, when compared with the general population.

Using univariate proportional hazards analysis, the researchers found that increasing age and hypertension were associated with an increased risk of incident MI after TIA. Notably, the use of lipid-lowering agents at the time of the TIA showed a trend toward association with an increased risk of MI after TIA.

However, on multivariable analysis, the researchers identified increasing age (hazard ratio, 1.51/10 years), male sex (HR, 2.19), and the use of lipid-lowering therapy at the time of TIA (HR, 3.10) to be independent risk factors for MI after TIA. TIA etiology was not a significant predictor, though this analysis was limited by the fact that a single etiology could not be identified in many patients.

"Our findings regarding the risk conferred by age and sex are consistent with the current understanding of CAD risk factors and pathogenesis," the investigators wrote. "Although hypertension is an important risk factor for CAD, its role as a risk factor for MI after TIA is unclear from our data." Effective treatment of hypertension could have obscured a difference in MI risk, they suggested.

On univariate analysis, the researchers found that patients who had an MI after a TIA were approximately three times more likely to die during follow-up than were those who did not have MI after TIA (HR, 3.19). Even when researchers adjusted for other factors found to be associated with mortality in this group, MI remained a significant and substantial independent predictor of death after TIA.

The authors acknowledged that the study has limitations. "Racial and ethnic differences exist in the epidemiology of CAD and ischemic cerebrovascular disease. Because the population of Rochester is predominantly white, our findings might not be applicable to other racial and ethnic groups."

There was also insufficient data available to assess the effects of lipid and cholesterol disorders – key CAD risk factors – on the risk of MI after TIA. Also, "the cohort size number of events may limit power to detect risk factors for MI after TIA."

The study was supported by the Mayo Clinic. The investigators did not report any relevant financial relationships. Dr. Burns is now affiliated with the departments of neurology and neurosurgery at Boston University.

Individuals who have had a transient ischemic attack are twice more likely than are those in the general population to have a myocardial infarction, indicating that TIA might be a significant risk factor for MI, according to a population-based study that was published online in Stroke on March 24.

In addition, "in the population of patients with TIA we studied, having MI increased the risk of death by a factor of three. This supports the concept of careful primary prevention of CAD [coronary artery disease] in TIA patients, even in the absence of symptoms. It also suggests that screening for CAD in at least some TIA patients may be reasonable," wrote Dr. Joseph D. Burns and his coinvestigators at the Mayo Clinic in Rochester, Minn. (Stroke 2011;42 [doi: 10.1161/STROKEAHA.110.593723]).

The researchers studied a community-based cohort of patients with incident TIA that was identified retrospectively through the Rochester Epidemiology Project Medical Records Linkage System, which holds medical record data for these individuals for all care provided, as well as and autopsy or death certificate information.

The investigators identified a cohort of Rochester residents who had incident TIA during 1985-1994 and a cohort of Olmsted County (Minn.) residents who had incident MI during 1979-2006.

A total of 456 Rochester residents had an incident TIA in 1985-1994. Of these, 15% (68) had a history of MI before TIA and were excluded from the analysis. Therefore the study results pertain to the 388 remaining patients.

On average, patients were 71 years old at the time of TIA and 41% of the patients were male. In terms of cardiovascular risk factors, 62% had hypertension, 11% had diabetes mellitus, and 55% were current or former smokers. Based on TOAST (Trial of ORG 10172 in Acute Stroke Treatment) subtypes, 19% of the TIAs were attributable to large artery atherosclerosis, 13% were cardioembolic, 6% were lacunar, and 5% were attributable to other causes. Importantly, a single etiology could not be clearly established for 57% of the TIAs.

Median follow-up for patients who had a TIA was 10 years. Of these, 44 patients had an MI after the TIA – an average annual incidence of MI after TIA of 0.95%. Median time from index TIA to index MI was 4.6 years. The risk of MI after TIA remained essentially constant over time, based on a survival analysis.

The age-, sex-, and period-specific relative risk for incident MI in patients who had TIA – when compared with that of the general population – was 2.09. Interestingly, this elevated risk was most pronounced in TIA patients younger than 60 years old. For those younger than 60 years, that relative risk was 15.1, when compared with the general population. In comparison, for patients 60 years and older, the age-, sex-, and period-specific relative risk for MI aggregated over three age groups (60-69 years, 70-79 years, and 80 years or older) was 1.93, when compared with the general population.

Using univariate proportional hazards analysis, the researchers found that increasing age and hypertension were associated with an increased risk of incident MI after TIA. Notably, the use of lipid-lowering agents at the time of the TIA showed a trend toward association with an increased risk of MI after TIA.

However, on multivariable analysis, the researchers identified increasing age (hazard ratio, 1.51/10 years), male sex (HR, 2.19), and the use of lipid-lowering therapy at the time of TIA (HR, 3.10) to be independent risk factors for MI after TIA. TIA etiology was not a significant predictor, though this analysis was limited by the fact that a single etiology could not be identified in many patients.

"Our findings regarding the risk conferred by age and sex are consistent with the current understanding of CAD risk factors and pathogenesis," the investigators wrote. "Although hypertension is an important risk factor for CAD, its role as a risk factor for MI after TIA is unclear from our data." Effective treatment of hypertension could have obscured a difference in MI risk, they suggested.

On univariate analysis, the researchers found that patients who had an MI after a TIA were approximately three times more likely to die during follow-up than were those who did not have MI after TIA (HR, 3.19). Even when researchers adjusted for other factors found to be associated with mortality in this group, MI remained a significant and substantial independent predictor of death after TIA.

The authors acknowledged that the study has limitations. "Racial and ethnic differences exist in the epidemiology of CAD and ischemic cerebrovascular disease. Because the population of Rochester is predominantly white, our findings might not be applicable to other racial and ethnic groups."

There was also insufficient data available to assess the effects of lipid and cholesterol disorders – key CAD risk factors – on the risk of MI after TIA. Also, "the cohort size number of events may limit power to detect risk factors for MI after TIA."

The study was supported by the Mayo Clinic. The investigators did not report any relevant financial relationships. Dr. Burns is now affiliated with the departments of neurology and neurosurgery at Boston University.

Individuals who have had a transient ischemic attack are twice more likely than are those in the general population to have a myocardial infarction, indicating that TIA might be a significant risk factor for MI, according to a population-based study that was published online in Stroke on March 24.

In addition, "in the population of patients with TIA we studied, having MI increased the risk of death by a factor of three. This supports the concept of careful primary prevention of CAD [coronary artery disease] in TIA patients, even in the absence of symptoms. It also suggests that screening for CAD in at least some TIA patients may be reasonable," wrote Dr. Joseph D. Burns and his coinvestigators at the Mayo Clinic in Rochester, Minn. (Stroke 2011;42 [doi: 10.1161/STROKEAHA.110.593723]).

The researchers studied a community-based cohort of patients with incident TIA that was identified retrospectively through the Rochester Epidemiology Project Medical Records Linkage System, which holds medical record data for these individuals for all care provided, as well as and autopsy or death certificate information.

The investigators identified a cohort of Rochester residents who had incident TIA during 1985-1994 and a cohort of Olmsted County (Minn.) residents who had incident MI during 1979-2006.

A total of 456 Rochester residents had an incident TIA in 1985-1994. Of these, 15% (68) had a history of MI before TIA and were excluded from the analysis. Therefore the study results pertain to the 388 remaining patients.

On average, patients were 71 years old at the time of TIA and 41% of the patients were male. In terms of cardiovascular risk factors, 62% had hypertension, 11% had diabetes mellitus, and 55% were current or former smokers. Based on TOAST (Trial of ORG 10172 in Acute Stroke Treatment) subtypes, 19% of the TIAs were attributable to large artery atherosclerosis, 13% were cardioembolic, 6% were lacunar, and 5% were attributable to other causes. Importantly, a single etiology could not be clearly established for 57% of the TIAs.

Median follow-up for patients who had a TIA was 10 years. Of these, 44 patients had an MI after the TIA – an average annual incidence of MI after TIA of 0.95%. Median time from index TIA to index MI was 4.6 years. The risk of MI after TIA remained essentially constant over time, based on a survival analysis.

The age-, sex-, and period-specific relative risk for incident MI in patients who had TIA – when compared with that of the general population – was 2.09. Interestingly, this elevated risk was most pronounced in TIA patients younger than 60 years old. For those younger than 60 years, that relative risk was 15.1, when compared with the general population. In comparison, for patients 60 years and older, the age-, sex-, and period-specific relative risk for MI aggregated over three age groups (60-69 years, 70-79 years, and 80 years or older) was 1.93, when compared with the general population.

Using univariate proportional hazards analysis, the researchers found that increasing age and hypertension were associated with an increased risk of incident MI after TIA. Notably, the use of lipid-lowering agents at the time of the TIA showed a trend toward association with an increased risk of MI after TIA.

However, on multivariable analysis, the researchers identified increasing age (hazard ratio, 1.51/10 years), male sex (HR, 2.19), and the use of lipid-lowering therapy at the time of TIA (HR, 3.10) to be independent risk factors for MI after TIA. TIA etiology was not a significant predictor, though this analysis was limited by the fact that a single etiology could not be identified in many patients.

"Our findings regarding the risk conferred by age and sex are consistent with the current understanding of CAD risk factors and pathogenesis," the investigators wrote. "Although hypertension is an important risk factor for CAD, its role as a risk factor for MI after TIA is unclear from our data." Effective treatment of hypertension could have obscured a difference in MI risk, they suggested.

On univariate analysis, the researchers found that patients who had an MI after a TIA were approximately three times more likely to die during follow-up than were those who did not have MI after TIA (HR, 3.19). Even when researchers adjusted for other factors found to be associated with mortality in this group, MI remained a significant and substantial independent predictor of death after TIA.

The authors acknowledged that the study has limitations. "Racial and ethnic differences exist in the epidemiology of CAD and ischemic cerebrovascular disease. Because the population of Rochester is predominantly white, our findings might not be applicable to other racial and ethnic groups."

There was also insufficient data available to assess the effects of lipid and cholesterol disorders – key CAD risk factors – on the risk of MI after TIA. Also, "the cohort size number of events may limit power to detect risk factors for MI after TIA."

The study was supported by the Mayo Clinic. The investigators did not report any relevant financial relationships. Dr. Burns is now affiliated with the departments of neurology and neurosurgery at Boston University.