Key result
Smoking after healed MI fails to increase cardiac output or stroke volume despite raising heart rate.
Why the study?
Does smoking affect cardiac output, stroke volume, and heart rate in subjects with healed myocardial infarction compared to normal subjects?
Observational
Does smoking affect cardiac output, stroke volume, and heart rate in subjects with healed myocardial infarction compared to normal subjects?
In patients with prior myocardial infarction, smoking increases heart rate but fails to increase cardiac output or stroke volume, suggesting different mediating factors for these hemodynamic responses.
Answers are grounded in this paper and cite their sources.
Hemodynamic dissociation after smoking in healed MI may signal impaired reserve; hypothesis-generating and should not yet change practice.
Smoking by subjects with healed myocardial infarction, in contrast to its effects on the normal subject, fails to provoke an increase in cardiac output or in stroke volume. On the other hand, smoking does increase the heart rate in subjects with healed myocardial infarction. This dissociation between the effect on heart rate and on cardiac output and stroke volume, which was also noted in the healthy subject pretreated with glucose, indicates that increase in heart rate is mediated by different factors than those that increase stroke volume and cardiac output.
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Frankl et al. (1965) conducted an observational in Healed Myocardial Infarction. Smoking vs. Normal subjects was evaluated on Cardiac output and stroke volume. Smoking in subjects with healed myocardial infarction fails to increase cardiac output or stroke volume, despite increasing heart rate, unlike its effects in normal subjects.
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