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Biomedical subjects

A D Timmis

Publications and source records attributed to A D Timmis.

At least 73 records · Page 4Linked to original sources
PubMed1994

Acute myocardial infarction in women: survival analysis in first six months.

OBJECTIVE: To examine the influence that being female has on the outcome of acute myocardial infarction. DESIGN: Observational follow up study. SETTING: London district general hospital. PATIENTS: 216 women and 607 men with acute myocardial infarction admitted to a coronary care unit from 1 January 1988 to 31 December 1992. MAIN OUTCOME MEASURES: All cause mortality and recurrent ischaemic events in the first six months. RESULTS: Event free survival (95% confidence interval) at six months was 63.3% (56.3% to 69.4%) in women and 76.1% (72.4% to 79.4%) in men, P < 0.001. The difference was confined to the first 30 days but thereafter the hazard plots for women and men converged, with reduction of the hazard ratio from 2.36 (1.70 to 3.27) to 0.81 (0.44 to 1.48). Women were older, but their excess risk persisted after adjustment for age, other baseline variables, and indices of severity of infarction (hazard ratio 1.53 (1.09 to 2.15), P = 0.015). Women tended to be treated with thrombolysis less commonly than men but the difference was small. Substantially fewer women than men, however, were discharged taking beta blockers (23.3% v 41.4%, P < 0.001), and although additional adjustment for discharge treatment did not further reduce the point estimate of the hazard ratio (1.84 (0.89-3.83)), the 95% confidence interval was wide and statistical significance was lost. CONCLUSIONS: Women with acute myocardial infarction have a worse prognosis than men but the excess risk is confined to the first 30 days and is only partly explained by age and other baseline variables. The tendency for women to receive less vigorous treatment than men must be remedied before gender can be considered to be an independent determinant of risk.

Adrenergic beta-Antagonists↗
PubMed1994

Relative value of clinical variables, treadmill stress testing, and Holter ST monitoring for postinfarction risk stratification.

The aim of this study was to compare the roles of clinical assessment, treadmill stress testing, and Holter ST analysis for postinfarction risk stratification in patients treated with thrombolysis. The study group consisted of 256 consecutive patients, all of whom underwent Holter ST monitoring early (mean 83 hours, range 48 to 180) after admission. Of these, 12 were excluded from the analysis either because Holter recordings were of insufficient quality (n = 6), or because reinfarction occurred within 24 hours of monitoring (n = 6). In the remaining 244 patients, 43 sustained a recurrent event (death, reinfarction, unstable angina) over the 8-month (range 3 to 12) follow-up period, and an additional 14 patients required revascularization. At multivariate event-free survival analysis, Killip class > or = 2 and Holter ST shift were independently predictive of the outcome. The strongest predictor was Holter ST shift at a cumulative duration of > 60 minutes. Of the 232 patients eligible for stress testing (12 sustained an event between Holter monitoring and the scheduled stress test), 196 were able to perform the test. The variable "inability to perform a stress test" was not independently predictive of outcome and did not influence the multivariate analysis. When clinical, Holter, and stress test variables were taken into account in patients who performed a stress test, Killip class was the only independent predictor of outcome (event-free survival). When revascularization was included as an end point, Holter ST shift was the only independent predictor of outcome. In conclusion, a significant proportion of recurrent events after thrombolysis occurs very early, before stress testing can be performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Early exercise testing after treatment with thrombolytic drugs for acute myocardial infarction: importance of reciprocal ST segment depression.

OBJECTIVE: To investigate the clinical importance of reciprocal ST depression induced by exercise testing early after acute myocardial infarction in patients treated with thrombolysis. DESIGN: Prospective observational study. SETTING: District general hospital in London. SUBJECTS: 202 patients (170 men) aged 33-69 with acute myocardial infarction treated with thrombolysis. MAIN OUTCOME MEASURES: All patients underwent exercise testing and coronary arteriography. ST depression induced by exercise was classified as either reciprocal (associated with ST elevation) or isolated (occurring on its own). The relation between reciprocal ST depression and the following end points was studied: characteristics of the infarct, left ventricular ejection fraction, extent of coronary artery disease on arteriography, and presence of angina induced by exercise. RESULTS: Reciprocal ST depression occurred almost exclusively in Q wave infarctions and was associated with a lower overall ejection fraction than isolated ST depression. It tended to be associated with persistent occlusion of the coronary artery related to the infarct and did not indicate remote ischaemia due to multivessel coronary disease. Unlike isolated ST depression, reciprocal ST depression was not associated with angina induced by exercise. CONCLUSIONS: Reciprocal ST depression induced by exercise is usually associated with extensive Q wave infarctions and persistent occlusion of the artery related to the infarct. It does not seem to indicate reversible ischaemia and should not be used as a non-invasive marker of multivessel disease in the assessment of requirements for further investigation soon after acute myocardial infarction.

Adult↗
PubMed1994

Relation between heart rate variability early after acute myocardial infarction and long-term mortality.

The relation between both time and frequency domain analyses of RR variability and mortality was examined in a series of 226 consecutive patients with acute myocardial infarction admitted to 3 district hospitals in London. All patients underwent 24-hour Holter monitoring early after infarction (mean 83 hours, range 48 to 180), and time and frequency domain analyses of RR variability were performed using commercially available software. During an 8-month follow-up period (range 3 to 12 months), there were 19 cardiac deaths (8.4%). Time domain analysis confirmed reduced RR variability (SDRR, SDANN, SD) among nonsurvivors compared with survivors. However, there was no difference between the groups when the percentage of absolute differences between successive RR intervals > 50 ms (pNN50) and the root-mean-square of successive differences (RMSSD)--vagal measures of RR variability--were analyzed. Frequency domain analysis demonstrated a significant difference between those who died and the survivors when the low-frequency component--modulated by both vagal and sympathetic mechanisms--was analyzed; however, this was less marked when the high-frequency component--modulated by vagal activity--was analyzed. None of these measures of RR variability was related to infarct site or left ventricular ejection fraction. In conclusion, the data confirm the association between low RR variability and mortality after acute myocardial infarction. However, the mechanism does not appear to relate exclusively to decreased parasympathetic tone. The data suggest that the increased risk of early mortality associated with reduced RR variability reflects an imbalance in sympathovagal function that is unrelated to left ventricular function.

Adult↗
PubMed1994

Mechanisms of cold intolerance in patients with angina.

OBJECTIVES: Patients with angina often report that symptoms are worse in cold weather. This study was designed to determine differences between cold-tolerant and cold-intolerant patients in the hemodynamic and ischemic response to exercise at cold temperatures and to assess the role of catecholamines and baroreceptor function. BACKGROUND: Studies have suggested that the heart rate response may differ at cold temperatures, but the mechanism and role of this variation have not been examined. METHODS: Seven cold-intolerant and seven cold-tolerant patients with angina underwent exercise treadmill testing at 6 and 25 degrees C with measurement of catecholamines. Baroreceptor function was assessed by the decrease in systolic blood pressure after patients stood up from the supine position. RESULTS: Norepinephrine levels increased by 139% in the cold environment, but there were no differences between cold-intolerant and cold-tolerant patients. Consequently, blood pressure was higher in the cold environment in all patients, but the heart rate response was similar. However, cold-intolerant patients had a steeper heart rate response in the cold and developed ischemia (mean [+/- SEM] 201 +/- 58 vs. 242 +/- 50 s, p = 0.05) and angina (348 +/- 87 vs. 449 +/- 60 s, p = 0.04) earlier in the cold environment, a difference not seen in the cold-tolerant patients. Baroreceptor function was impaired in cold-intolerant patients (decrease in systolic blood pressure after patients stood up from the supine position 19 +/- 7 vs. 0 +/- 4 mm Hg, p = 0.04). CONCLUSIONS: Exposure to cold causes an increase in blood pressure with an associated increase in myocardial oxygen demand in all patients. In cold-tolerant patients, this increase may be offset by a reduction in heart rate if baroreceptor function is normal. If baroreceptor function is abnormal, heart rate may not decrease in response to a cold-induced increase in blood pressure. This mechanism may account for some of the variability in tolerance to cold exposure that affects patients with exertional angina.

Angina Pectoris↗
PubMed1994

Reexamination of the role of endogenous opiates in silent myocardial ischemia.

OBJECTIVES: This study was designed to examine the role of beta-endorphin and met-enkephalin in the pathophysiology of silent myocardial ischemia, with emphasis on their role in the physiologic response to stress. BACKGROUND: Silent myocardial ischemia is more common in patients whose perception of pain is reduced. Whether endogenous opiates can contribute to this process remains uncertain largely because of the conflicting findings of previous studies. METHODS: Forty-three patients with coronary artery disease and ischemia on treadmill stress testing underwent electrical pain tests and exercise treadmill tests during naloxone and placebo infusion in a randomized, double-blind crossover study. Thirty-one patients developed angina during both treadmill tests (group A), and 12 had silent ischemia (group B). Plasma beta-endorphin, metenkephalin, epinephrine, norepinephrine and cortisol were measured before and after exercise in a subgroup of 17 patients. RESULTS: Naloxone reduced electrical pain tolerance (1.40 +/- 0.10 [mean +/- SEM] vs. 1.72 +/- 0.19 mA, p = 0.04) but did not affect the time to angina in group A (260 +/- 20 vs. 248 +/- 20 s, p = 0.72) or induce angina in group B patients. Beta-endorphin and met-enkephalin levels during placebo infusion were not significantly different in groups A and B at baseline and after exercise, although beta-endorphin levels were significantly increased during naloxone infusion, confirming effective opiate receptor blockade. Norepinephrine and cortisol increased with exercise, but catecholamines and cortisol were similar in both groups and were unaffected by naloxone. CONCLUSIONS: Beta-endorphin and met-enkephalin were similar in patients with painful and silent ischemia, and naloxone infusion did not influence anginal symptoms despite effective opiate receptor blockade and a reduction in somatic pain tolerance. These findings suggest that endogenous opiates do not play an important role in modulating symptoms in myocardial ischemia. The increase in beta-endorphin with exercise that coincided with an increase in plasma cortisol is most likely due to its release from the anterior pituitary gland as part of the physiologic stress response.

Double-Blind Method↗
PubMed1994

Failure of epoprostenol (prostacyclin, PGI2) to inhibit platelet aggregation and to prevent restenosis after coronary angioplasty: results of a randomised placebo controlled trial.

OBJECTIVE: To study the effect of epoprostenol (prostacyclin, PGI2) given before, during, and for 36 h after coronary angioplasty on restenosis at six months and to evaluate the transcardiac gradient of platelet aggregation before and after percutaneous transluminal coronary angioplasty (PTCA) in treated and placebo groups. DESIGN: Double blind placebo controlled randomised study. PATIENTS: 135 patients with successful coronary angioplasty. METHODS: Intravenous infusion of PGI2 (4 ng/kg/ml) or buffer was started before balloon angioplasty and continued for 36 hours. Platelet aggregation was measured in blood from the aorta and coronary sinus before and after PTCA in each group. Routine follow up was at six months with repeat angiography and there was quantitative assessment of all angiograms (those undertaken within the follow up period and at routine follow up). PRESENTATION OF RESULTS: Restenosis rates in treated and placebo groups determined according to the National Heart, Lung and Blood Institute definition IV. Comparison at follow up between the effect of treatment on mean absolute luminal diameter and mean absolute follow up diameter in the placebo group. Comparison of acute gain and late loss between groups. RESULTS: Of 125 patients available for assessment 23 were re-admitted because of angina within the follow up period. Quantitative angiography showed restenosis in 15 (10 in the PGI2 group and five in the placebo group). Of 105 patients evaluated at six month angiography there was restenosis in nine more in the PGI2 group and 18 more in the placebo group. Total restenosis rates (for patients) were 29.2% for PGI2 and 38.3% for placebo (NS). The mean absolute gain in luminal diameter was 1.84 (0.76) mm in the PGI2 group and 1.58 (0.56) mm in the placebo group (p = 0.04); the late loss in the PGI2 group was also greater (0.65 (0.94) mm vs 0.62 (0.89) mm (NS) and there was no significant difference in final luminal diameter at follow up between the two groups (1.83 (0.88) mm v 1.59 (0.60) mm). The transcardiac gradient of quantitative platelet aggregation increased after PTCA in both groups, indicating that PGI2 in this dose did not affect angioplasty-induced platelet activation. Mean (SD) platelet activation indices in the PGI2 group were pre PTCA aorta 8.4 (4.1) v coronary sinus 8.8 (4.0) (p = 0.001) and post PTCA aorta 8.9(3.0) v coronary sinus 12.9 (5.7) (p = 0.001). In the placebo group the values were pre PTCA aorta 7.6 (3.3) v coronary sinus 7.4 (3.6) (p = 0.001) and post PTCA aorta 7.6(2.8) v coronary sinus 11.2(4.3) (p = 0.001). CONCLUSION: The dose of PGI2 given was designed to limit side effects and as a short-term infusion did not significantly decrease the six month restenosis rate after PTCA. The sample size, which was determined by the original protocol and chosen because of the potency of the agent being tested, would have detected only a 50% reduction in restenosis rate. There was, however, no effect in the treated patients on the increased platelet aggregation seen in placebo group as a result of angioplasty. Angioplasty is a powerful stimulus to blood factor activation. Powerful agents that prevent local platelet adhesion and aggregation are likely to be required to reduce restenosis.

Angioplasty, Balloon, Coronary↗
PubMed1994

Influence of the autonomic nervous system on circadian patterns of myocardial ischaemia: comparison of stable angina with the early postinfarction period.

OBJECTIVE: To compare the circadian rhythm of myocardial ischaemia in patients with stable angina with that in patients in the early postinfarction period with particular emphasis on the role of the autonomic nervous system. PATIENTS: 44 patients with stable angina and ischaemia on treadmill testing (group A) were compared with 131 patients in the early postinfarction period (group B). All had 48 hour ambulatory Holter monitoring. SETTING: Coronary care unit and cardiology department of a district general hospital. DESIGN: Prospective, between group, comparative study. RESULTS: 337 ischaemic episodes occurred in 35 patients in group A and 370 ischaemic episodes occurred in 65 patients in group B. 34% of patients in group A had only silent episodes of ischaemia compared with 97% in group B (p < 0.0001). In group A ischaemic episodes showed a circadian rhythm that peaked during the daytime hours (p < 0.0001), but this was not seen in group B. Both the high (0.15-0.40 Hz) and low (0.04-0.15 Hz) frequency spectral components of heart rate variability showed a clear circadian rhythm (p < 0.0001); peak values occurred during the sleeping hours, although this pattern was less pronounced in group B. The ratio of low to high frequency variability (a measure of sympathovagal balance) showed a peak in daytime hours in group A (p < 0.002), but this was not seen in group B. CONCLUSION: In stable angina, myocardial ischaemia peaks during the day and is associated with a similar circadian rhythm of sympathovagal balance. In the early postinfarction period both the ischaemic and sympathovagal rhythms are severely diminished or lost altogether. Circadian changes in sympathovagal tone may explain, at least in part, the circadian rhythm of ambulatory myocardial ischaemia in patients with stable angina.

Angina Pectoris↗
PubMed1994

Emergency surgical revascularisation for coronary angioplasty complications.

OBJECTIVES: To evaluate trends in referrals for emergency operations after percutaneous transluminal coronary angioplasty (PTCA) complications; to analyse morbidity and mortality and assess the influence of PTCA backup on elective surgery. DESIGN: A retrospective analysis of patients requiring emergency surgical revascularisation within 24 hours of percutaneous transluminal coronary angioplasty. PATIENTS: Between January 1980 and December 1990, 75 patients requiring emergency surgery within 24 hours of percutaneous transluminal coronary angioplasty. SETTING: A tertiary referral centre and postgraduate teaching hospital. RESULTS: 57 patients (76%) were men, the mean age was 55 (range 29-73) years, and 30 (40%) had had a previous myocardial infarction. Before PTCA, 68 (91%) had severe angina, 59 (79%) had multivessel disease, and six (8%) had a left ventricular ejection fraction of less than 40%. A mean of 2.1 grafts (range one to five) were performed; the internal mammary artery was used in only one patient. The operative mortality was 9% and inhospital mortality was 17%. There was a need for cardiac massage until bypass was established in 19 patients (25%): this was the most important outcome determinant (P = 0.0051) and was more common in those patients with multivessel disease (P = 0.0449) and in women (P = 0.0388). In 10 of the 19 cases a vacant operating theatre was unavailable, the operation being performed in the catheter laboratory or anaesthetic room. These 19 patients had an operative mortality of 32% and inhospital mortality of 47%, compared with 2% and 7% respectively for the 56 patients who awaited the next available operating theatre. Complications included myocardial infarction, 19 patients (25%); arrhythmias, 10 patients (3%); and gross neurological event, two patients (3%). The mean intensive care unit stay was 2.6 days (range 1 to 33 days) and the mean duration of hospital admission was 13 days (range 5-40 days). CONCLUSIONS: Patients undergoing emergency surgery after PTCA complications have a substantially increased inhospital mortality and morbidity. PTCA in this unit continues to require surgical cover. Delays in operating on stable patients in centres which operate a "next available theatre" backup policy may not differ from some units performing PTCA with offsite cover for PTCA complications. Particularly in the presence of multivessel disease, however, PTCA complications may be associated with the need for "crash" bypass and such patients are unlikely to survive hospital transfer. The proportion of patients requiring "crash" bypass has increased during the period reviewed because of the extent of disease in the emergency surgical group increased. These results indicate that surgery should not be denied to these patients.

Adult↗
PubMed1993

Silent myocardial ischemia: role of subclinical neuropathy in patients with and without diabetes.

OBJECTIVES: Silent myocardial ischemia is common in patients with diabetes. This study was designed to assess the role of subclinical autonomic impairment in diabetic patients with silent ischemia. BACKGROUND: Studies have suggested that silent ischemia is more common in diabetic patients with microvascular complications, but this has not been a consistent finding. METHODS: Twenty-two diabetic and 30 nondiabetic patients with proved coronary artery disease and a history of angina and ischemia on treadmill stress testing underwent clinical tests of autonomic function and measurement of 24-h heart rate variability. Diabetic patients with a history of microvascular complications were excluded. RESULTS: Although all 52 patients manifested ischemia during treadmill testing, only 36 patients experienced angina (angina group), whereas 16 did not (silent ischemia group). Diabetic and nondiabetic patients were similar in age (59 +/- 1 vs. 61 +/- 2 years, p = 0.56) and extent of coronary artery disease. However, clinical tests showed reduced parasympathetic function in the diabetic patients (Valsalva ratio 1.38 +/- 0.07 vs. 1.60 +/- 0.06; p = 0.007). Patients in the silent ischemia group were more often diabetic (33% vs. 63%, p = 0.05) and had prolonged time to ischemia on treadmill testing (200 +/- 20 vs. 271 +/- 20 s, p = 0.03). In addition, autonomic function was impaired in the silent group (supine/standing heart rate ratio 1.15 +/- 0.02 vs. 1.05 +/- 0.02, p = 0.002). Subgroup analysis showed that abnormalities of autonomic function were confined to the diabetic patients in the silent group. CONCLUSIONS: Despite the absence of overt microvascular complications, diabetic patients with silent exertional ischemia have evidence of significant autonomic impairment compared with findings in symptomatic patients. This difference is not seen in nondiabetic patients and indicates that subclinical neuropathy is an important cause of silent ischemia in patients with diabetes.

Adult↗
PubMed1993

Short and long term prognosis of acute myocardial infarction since introduction of thrombolysis.

OBJECTIVE: To record prognosis and determinants of outcome in patients with acute myocardial infarction since thrombolysis was introduced. DESIGN: Observational study. SETTING: London district general hospital. PATIENTS: 608 consecutive patients admitted to the coronary care unit with acute myocardial infarction between 1 January 1988 and 31 December 1991. MAIN OUTCOME MEASURE: All cause mortality, non-fatal ischaemic events (myocardial infarction, unstable angina), and revascularisation. RESULTS: Of the 608 patients, 89 (14.6%) died in hospital. 507 [corrected] patients were followed up after discharge from hospital. Mortality (95% confidence interval) at 30 days, one year, and three years was 16.0% (13.4% to 19.2%), 21.7% (18.6% to 25.2%), and 29.4% (25.3% to 33.9%) respectively. Event free survival (survival without a non-fatal ischaemic event) was 80.4% (77.0% to 83.4%) at 30 days, 66.8% (62.8% to 70.5%) at one year, and 56.1% (51.3% to 60.6%) at three years. Survival in patients treated with thrombolysis was considerably higher than in those not given thrombolysis (three year survival: 76.7% v 54.3%), although the incidence of non-fatal ischaemic events was the same in the two groups. Multivariate determinants of six month survival were left ventricular failure, treatment with thrombolysis and aspirin, smoking history, bundle branch block, and age. For patients who survived six months, age was the only factor related to long term survival. CONCLUSIONS: Although patients treated by thrombolysis had a relatively good prognosis, long term mortality and the incidence of non-fatal recurrent ischaemic events remained high. Effective strategies for the identification and treatment of high risk patients need to be reassessed.

Age Factors↗
PubMed1993

Free radical activity and left ventricular function after thrombolysis for acute infarction.

BACKGROUND: Experimental data suggest that reperfusion injury involving free radicals contributes to the impairment of left ventricular function after successful thrombolysis. METHODS: In 72 patients presenting with acute myocardial infarction, markers of free radical activity were measured before streptokinase and two hours later. Thiobarbituric acid reactive material (TBA-RM) reflects lipid peroxidation by free radicals, and the concentration of plasma total thiols (34 patients) reflects oxidative stress. Coronary arteriography was performed at 18-72 hours after thrombolysis to determine coronary patency, and left ventricular function was assessed by ventriculography and from QRS scoring of the electrocardiogram. RESULTS: The infarct related artery was patent (Thrombolysis In Myocardial Infarction Trial grade 2 or better) in 60 (83%) and occluded in 12. In the 60 with a patent artery, the concentration of TBA-RM increased after streptokinase by (mean (SD)) 9.2 (14.0) nmol/g albumin, whereas in the 12 with an occluded artery TBA-RM decreased by 7.0 (11.3) nmol/g albumin (p < 0.01 between groups). In those with a patent artery the rise in TBA-RM associated with thrombolysis correlated with left ventricular ejection fraction (R = -0.41, p < 0.002), and with the QRS score (R = +0.38, p = 0.003). Plasma total thiol concentrations decreased by 12.7 (31.1) mumol/l in those with a patent artery, and this decrease associated with thrombolysis correlated with left ventricular ejection fraction (R = +0.39, p < 0.02) but not with the QRS score (R = -0.2, NS). CONCLUSIONS: These findings suggest that reperfusion injury mediated by free radicals may be of clinical importance in humans.

Adult↗
PubMed1993

Significance of reciprocal ST depression in acute myocardial infarction: a study of 258 patients treated by thrombolysis.

OBJECTIVE: To investigate the clinical significance of reciprocal ST depression on the presenting electrocardiogram in patients with acute myocardial infarction treated by thrombolysis. DESIGN: A prospective cohort analytical study. SETTING: A London district general hospital. SUBJECTS: Two hundred and fifty eight consecutive patients with acute myocardial infarction treated with thrombolysis. INTERVENTIONS: All patients underwent treadmill stress testing after a mean (SEM) of 10 (3) days; 200 patients (78%) were referred for coronary arteriography at 30 (16) days. MAIN OUTCOME MEASURES: Relation between reciprocal ST depression at presentation and several endpoints: time from start of chest pain to hospital presentation, electrocardiographic changes during early treadmill stress testing, presence of multivessel coronary disease, and clinical outcome in terms of recurrent ischaemic events (death, reinfarction, and unstable angina) during a 10 (range six to 12) month follow up. RESULTS: Presentation was generally early, but in this group of patients reciprocal ST depression was significantly related to the time from the start of symptoms, those with reciprocal change presenting on average one hour earlier than those without. Although reciprocal change on the presenting electrocardiogram was weakly associated with ST depression on treadmill stress testing, it was not indicative of remote ischaemia as a result of multivessel coronary disease or high grade collateralisation of the infarct related artery. There was no association between reciprocal change and the incidence of recurrent ischaemic events. CONCLUSION: Reciprocal ST depression on the presenting electrocardiogram seems to be a benign electrical phenomenon related to the time from the start of symptoms. It does not necessarily predict an adverse prognosis in patients treated by thrombolysis.

Adult↗
PubMed1993

Circadian and seasonal factors in the pathogenesis of acute myocardial infarction: the influence of environmental temperature.

OBJECTIVE: To determine the circadian and seasonal variations in the incidence of acute myocardial infarction and the influence of environmental temperature. PATIENTS: 633 consecutive patients with acute myocardial infarction admitted to a coronary care unit over four years. SETTING: Coronary care unit in a district general hospital. DESIGN: An observational study. RESULTS: The onset of acute myocardial infarction had a circadian rhythm with a peak in the second quarter of the day. A seasonal variation was also found with a significant winter peak. There was, however, an excess of infarctions on colder days in both winter and summer indicating that the effect of environmental temperature on the onset of acute myocardial infarction is independent of the time of year. CONCLUSION: Acute myocardial infarction is more common in winter and more common on colder days, independent of season. Environmental temperature may play an important part in the pathogenesis of acute myocardial infarction.

Adult↗