The concept of ‘triggering’ for acute myocardial infarction (AMI) emerged almost a century ago when Obraztsov and Strazhesko provided anecdotal evidence stating that ‘direct events,’ such as psychological stress or physical activity, could precipitate acute myocardial infarction. Some of the recognized psychological triggers include:
Anger has been found to be associated with increased risk AMI. Mittleman and colleagues reported that anger level corresponding with “very angry, body tense, clenching fists or teeth,” up to “furious or enraged,” was associated with a transient two-hour risk increase of 2.3-fold increase of AMI (95% CI 1.2 to 3.2) above baseline when the control was usual annual frequency. The most frequent reported contributors to anger were arguments with family members (25%), conflicts at work (22%), and legal problems (8%).39
Several well-documented physiological effects of anger make the hypothesis of triggering of myocardial infarction by an outburst of anger biologically plausible. It has been demonstrated that mental stress can increase heart rate, blood pressure, and myocardial oxygen demand.40 These effects are mediated at least in part by catecholamine secretion.40 Verrier and colleagues have reported that anger, induced in a dog model, elicited increases in coronary vascular resistance and ischemic ST segment changes.41 It has also been shown that recall of an incident that elicited anger was more potent than other mental stressors or exercise in triggering myocardial ischemia, as measured by a reduction in left ventricular ejection fraction in patients with documented coronary artery disease.42 In addition to hemodynamic effects, mental stress also has been shown to increase platelet aggregability.43
An elevated relative risk of 1.6 (95% CI 1.1 to 2.2) was associated with episodes of marked anxiety above the 75th percentile on an anxiety scale within the two hours before MI.39
Even stress regarding sports has been implicated as an acute trigger for AMI. Wilbert-Lampen and colleagues evaluated the risk of cardiovascular events in a German population during world Cup games when German national team played. Acute cardiovascular events were assessed in 4,279 patients. On days of matches involving the German team, the incidence of cardiac emergencies increased 2.66 times (3.26 times in men and 1.82 in women). Of those presenting with coronary events 47% had known CHD. The highest average incidence of events was observed during the first two hours after the beginning of each match. Risk of ST elevation MI was 2.49 times higher than control period. Non-ST elevation MI increased by 2.61.44
In a prospective study of 95,647 Finnish men and women, the risk of all-cause mortality in the first week following spousal death was two times normal. The risk of any ischemic heart disease event in that period was elevated 2.3-fold in men and 3.5-fold in women, an effect independent of age; the risk diminished dramatically by the end of the first month.45
In the week after the Los Angeles, California, earthquake of 1994, there was a 35% increase in nonfatal MI compared with the week before and a four-fold increase in sudden cardiac death on the day of the earthquake. For the six days after this spike, however, the number of sudden deaths fell below the baseline, which suggests that some of the initial deaths may have been moved forward by several days in individuals who were predisposed, rather than being excess deaths.46
Psychiatric disorders are common among patients with CHD. There is growing evidence that these disorders affect the overall prognosis of these patients. Recognition and treatment of psychiatric disorders in patients with CHD should be viewed as an integral part comprehensive treatment of CHD.
There remains uncertainty regarding whether psychiatric disorders can independently cause CHD or whether these disorders are merely risk markers for maladaptive behaviors, which affect compliance with therapy and eventually outcomes. Irrespective whether the relationship is causal or not, there is a need for improved recognition and treatment of psychiatric disorders. This early recognition and treatment of these disorders will have profound effect on patient’s overall well-being and health which may include deceasing risks of CHD.
|Explore More In Our Hep C Learning Center
What Is Hepatitis C?
Learn about this treatable virus.
Diagnosing Hepatitis C
Getting tested for this viral infection.
Just Diagnosed? Here’s What’s Next
3 key steps to getting on treatment.
Understanding Hepatitis C Treatment
4 steps to getting on therapy.
Your Guide to Hep C Treatments
What you need to know about Hep C drugs.
Managing Side Effects of Treatment
How the drugs might affect you.
Making Hep C Treatment a Success
These tips may up your chances of a cure.