Triggers Of Acute Myocardial Infarction Research Articles

Disparate effects of the 1989 Loma Prieta and 1994 Northridge earthquakes on hospital admissions for acute myocardial infarction: Importance of superimposition of triggers

Background Most occurrences of presumed triggers of acute myocardial infarction (AMI) do not actually trigger an AMI. The relation between vulnerability to development of AMI and timing of triggers of AMI is poorly understood. The 1989 Loma Prieta earthquake struck the San Francisco Bay Area at 5:04 PM during a period of relatively reduced circadian vulnerability to AMI. The 1994 Northridge earthquake awakened citizens of Los Angeles at 4:31 AM, also during a period of otherwise reduced vulnerability to AMI, but superimposed the stress of the earthquake upon the known stress of awakening. Study of times of onset of natural disasters and their effect on precipitation of AMI may provide insight into the physiology of triggering. This study was designed to compare the triggering ability of 2 similarly intense earthquakes that occurred singly or superimposed upon another trigger. Methods and Results California discharge records were analyzed from the week before, the day of, and the 6 days after the Loma Prieta and Northridge earthquakes and the same dates of control years for total admissions, AMI admissions, and congestive heart failure admissions. There was no statistically significant increase in AMI admissions in the San Francisco Bay Area on the day of the Loma Prieta earthquake compared with the days before or after the earthquake or compared with the same day in 1990. In contrast, there was a 110% increase in admission rate for AMI in Los Angeles County on the day of the Northridge earthquake compared with the average of the 7 days before the earthquake (z = 4.349, P < .001). Similarly, there was a >80% increased risk of admission for AMI on the day of the Northridge earthquake in 1994 compared with the same date in 1995 (relative risk 1.828, 95% confidence intervals 1.289 to 2.592). Conclusions Extreme emotional stress superimposed on the stress of awakening results in enhanced triggering of AMI. When emotional stress occurs at less vulnerable periods, there is no significant increase in incidence of AMI. (Am Heart J 1999;137:830-6.)

Cocaine Use as a Trigger of Acute Myocardial Infarction

Cocaine Use as a Trigger of Acute Myocardial Infarction

Cocaine use as a trigger of acute myocardial infarction

Cocaine use as a trigger of acute myocardial infarction

Hanshin-Awaji earthquake as a trigger for acute myocardial infarction

On Jan. 17, 1995, the Hanshin-Awaji district was struck by the most destructive earthquake ever to occur in Japan. It is commonly believed that acute emotional stress such as that caused by an earthquake can trigger acute myocardial infarction (AMI). The objective of this study was to evaluate the effect of the quake stress on the onset of AMI in our district. The number of patients with AMI during the first 4 weeks after the quake increased by about 3.5-fold. The mean age of patients was 72.5 +/- 2.8 years, and the proportion of women (53%) was significantly greater than in the preceding years. The proportion of patients without prodromal angina pectoris was 53%. The mean post-traumatic stress disorder reaction index score (n = 14) was 40.1 +/- 4.1, which indicates a severe stress level. The mean score in the women (45.9 +/- 4.7; n = 7) was significantly higher than that in the men (34.3 +/- 6.4; n = 7). We concluded that after an earthquake, severe emotional stress can trigger AMI, more often than normal in women.

Triggers of acute myocardial infarction regarding its site

We have studied the incidence of possible triggers of the myocardial infarction regarding its site in 750 patients with anterior and 731 patients with inferior infarction. Infarctions occurred most frequently without recalling any triggering activity, especially in patients with anterior infarction (67 vs. 44%). Physical effort as the possible precipitator was also more frequent in anterior infarctions (22 vs. 16%). However, the onset of inferior infarction was more frequent during meteorological stress (9 vs. 2%), emotional stress (10 vs. 3%), after overeating (13 vs. 3%) and nicotine abuse (6 vs. 1.5%). These triggers were independent and highly significant ( P<0.02 in each case) discriminators of the site of myocardial infarction. Bimodal circadian rhythm, with primary peak between 6 and 9 h a.m. and the secondary peak between 3 and 6 p.m. was observed in patients which did not recall any triggering activity, and this was more pronounced in patients with inferior infarction. These results support the hypothesis that the influence of the vegetative tone is most pronounced in the onset of myocardial infarction of inferior wall.

The Northridge earthquake as a trigger for acute myocardial infarction: Leor J, Kloner RA. Am J Cardiol. 1996;77:1230–1232

The Northridge earthquake as a trigger for acute myocardial infarction: Leor J, Kloner RA. Am J Cardiol. 1996;77:1230–1232

The Northridge earthquake as a trigger for acute myocardial infarction

The clinical implication of our study is that hospitals and emergency services should have contingency plans for increasing coronary care unit admissions and myocardial infarctions following an earthquake.

Snow shoveling: A trigger for acute myocardial infarction and sudden coronary death

Snow shoveling: A trigger for acute myocardial infarction and sudden coronary death

924-118 The January 17,1994 Los Angeles Earthquake as a Trigger for Acute Myocardial Infarction

The January 17, 1994 Los Angeles earthquake (EQ) provided a unique opportunity to examine the effect of extensive environmental disaster associated with tremendous emotional stress on the incidenCe of acute cardiac events. We surveyed 75 coronary care units (CCUs) in Southern California comparing the number of admissions for myocardial infarction (MI), unstable angina (UA), total CCU admissions and related in-hospital mortality in the week before (Jan 10–16) and after (Jan 17–23) the EQ. Five CCUs were excluded because of insufficient data. The relative risk for MI following the EQ was assessed in a subgroup of 29 CCUs that were able to provide data on the equivalent period in 1993. Total number of pts (average number ± SD per CCU): cases Week Before Week After p Value MI 147 (2.1 ± 2.7) 195 (2.9 ± 3.1) 0.01 UA 255 (3.6 ± 5.2) 273 (3.9 ± 5.2) 0.39 Total CCU pts 1096 (15.7 ± 13.2) 1174(16.8 ± 13.2) 0.18 The % of CCU admissions for Ml increased in the week following the EQ [195 of 1174 (16.6%) vs. 147 of 1096 (13.4%); P = 0.04]. The % of CCUs reporting increased number of MIs was higher in hospitals located within 15 miles of the EQ epicenter vs. hospitals located &gt; 15 miles [11 of 14 (79%) vs. 23 of 56(41%); p = 002]. In-hospital mortality (%) was similar for Ml and UA pts in the week before and after the EQ (Ml: 7% vs. 6%; UA: 1% vs. 0%, respectively). In comparison to 1993 (subgroup of 29 CCUs), there was a significant increase in the risk of developing MI in the week following the EQ vs. the week before (1994: 70 vs. 41 pts; 1993: 49 vs. 68 pts, respectively; odds ratio 2.4, 95% confidence interval 1.4 – 4.0). 1) Our data indicate a significant increase in the incidence of Ml but not UA or in hospital mortality in the week following the EQ. 2) Our observation supports the concept that a stressful event can trigger acute MI.

Physical Exertion as a Trigger of Acute Myocardial Infarction

Physical Exertion as a Trigger of Acute Myocardial Infarction

Triggering of Acute Myocardial Infarction by Heavy Physical Exertion: Protection against Triggering by Regular Exertion

Triggering of Acute Myocardial Infarction by Heavy Physical Exertion: Protection against Triggering by Regular Exertion

Triggering of Acute Myocardial Infarction by Heavy Physical Exertion

Triggering of Acute Myocardial Infarction by Heavy Physical Exertion

Triggering of acute myocardial infarction by heavy physical exertion. Protection against triggering by regular exertion. Determinants of Myocardial Infarction Onset Study Investigators.

Despite anecdotal evidence suggesting that heavy physical exertion can trigger the onset of acute myocardial infarction, there have been no controlled studies of the risk of myocardial infarction during and after heavy exertion, the length of time between heavy exertion and the onset of symptoms (induction time), and whether the risk can be modified by regular physical exertion. To address these questions, we collected data from patients with confirmed myocardial infarction on their activities one hour before the onset of myocardial infarction and during control periods. Interviews with 1228 patients conducted an average of four days after myocardial infarction provided data on their usual annual frequency of physical activity and the time, type, and intensity of physical exertion in the 26 hours before the onset of myocardial infarction. We compared the observed frequency of heavy exertion (6 or more metabolic equivalents) with the expected values using two types of self-matched analyses based on a new case-crossover study design. The low frequency of heavy exertion during the control periods was validated by data from a population-based control group of 218 subjects. Of the patients, 4.4 percent reported heavy exertion within one hour before the onset of myocardial infarction. The estimated relative risk of myocardial infarction in the hour after heavy physical exertion, as compared with less strenuous physical exertion or none, was 5.9 (95 percent confidence interval, 4.6 to 7.7), Among people who usually exercised less than one, one to two, three to four, or five or more times per week, the respective relative risks were 107 (95 percent confidence interval, 67 to 171), 19.4 (9.9 to 38.1), 8.6 (3.6 to 20.5), and 2.4 (1.5 to 3.7). Thus, increasing levels of habitual physical activity were associated with progressively lower relative risks. The induction time from heavy exertion to the onset of myocardial infarction was less than one hour, and symptoms usually began during the activity. Heavy physical exertion can trigger the onset of acute myocardial infarction, particularly in people who are habitually sedentary. Improved understanding of the mechanisms by which heavy physical exertion triggers the onset of myocardial infarction and the manner in which regular exertion protects against it would facilitate the design of new preventive approaches.

Modifiers of timing and possible triggers of acute myocardial infarction in the thrombolysis in myocardial infarction phase II (TIMI II) study group

Objectives. The aim of this study was to provide insight into the mechanism of acute myocardial infarction by determining the modifiers of timing and possible triggers of onset of infarction.Background. A higher frequency of onset of acute myocardial infarction has been reported in the morning with a peak in the 1st 3 h after awakening. This observation suggests that the onset of infarction may be triggered by activity in the morning and at other times ot the day.Methods. The clinical history of the 3,339 patients entered into the Thrombolysis in Myocardial Infarction phase II study was analyzed to determine characteristics predicting a higher frequency of infarction between 6 amand noon, and onset of infarction during exertion.Results. A higher proportion (34.4%) of infarctions began in the morning (6 amto noon) compared with other limes of the day. Characteristics independently predicting a higher frequency between 6 amto noon were no beta-adrensrgic blocking agent use in the 24 h before infarction, no discomfort other than the index pain in the preceding 48 h, occurrence of the infarction on a weekday and no history of current smoking.In 18.7% of patients, infarction occurred during moderate or marked physical activity. Independent predictors cf exertion-related infarction included male gender, bo history of current smoking, while race, no use of calcium channel blocking agents or nitrates in the preceding 24 h, the absence of either chest pain at rest in the 3 weeks before infarction or any pain in the preceding 48 h, the absence of new onset angina and the presence of exertional pain in the preceding 3 weeks. Compared with patients whose infarction occurred at rest or during mild activity, those with exertion-related infarction had fewer coronary vessels with ≥60% stenosis (p = 0.002) and were more likely to have an occluded infarct-related vessel after thrombolytic therapy (p = 0.01).Conclusions. Further study of the timing and activity at onset of infarction may provide insight into the pathophysiologic mechanisms causing acute myocardial infarction and provide clues to preventive measures.

Rupture of coronary vasa vasorum as a trigger of acute myocardial infarction

Some controversy has always existed regarding the presence and extent of the vasa vasorum—the nutrient vessels in the wall of the human aorta—in the coronary arteries. Now, cinemicrographic studies using silicone polymer injections in cleared human hearts have identified the vasa vasorum of coronary arteries, revealing evidence of neovascularization in the region of atherosclerotic plaques. These studies suggest an important role for the vasa vasorum in the pathogenesis of coronary atherosclerosis and its sequelae, especially intramural hemorrhage and vascular spasm. The wall of the human coronary artery in regions of atherosclerotic injury may be particularly rich in capillary vessels of the vasa vasorum. From this, the evidence suggests that with the morning increase in blood pressure, fragile neovascular structures of the vasa vasorum may be more prone to rupture and may be responsible, in part, for the circadian variation in myocardial infarction.

Analysis of possible triggers of acute myocardial infarction (the MILIS study)

Recent documentation of a circadian variation in acute myocardial infarction (AMI) suggests that AMI is not a random event, but may frequently result from identifiable triggering activities. The possible triggers reported by 849 patients enrolled in the Multicenter Investigation of Limitation of Infarct Size were analyzed. Possible triggers were identified by 48.5% of the population; the most common were emotional upset (18.4%) and moderate physical activity (14.1%). Multiple possible triggers were reported by 13% of the population. Younger patients, men and those without diabetes mellitus were more likely to report a possible trigger than were older patients, women and those with diabetes. The likelihood of reporting a trigger was not affected by infarct size. This study suggests that potentially identifiable triggers may play an important role in AMI. Because potential triggering activities are common in persons with coronary artery disease, yet infrequently result in AMI, further studies are needed to identify (1) the circumstances in which a potential trigger may cause an event, (2) the specific nature of potential triggering activites, (3) the frequency of such activities in individuals who do not develop AMI and (4) the presence or absence of identifiable triggers in various subgroups of patients with infarction.