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Tuesday, January 8, 2008
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Dietary: Cerebral and Myocardial Infarctions
Association of Dietary Intake of Soy, Beans, and Isoflavones With Risk of Cerebral and Myocardial Infarctions in Japanese Populations
Yoshihiro Kokubo, MD; Hiroyasu Iso, MD; Junko Ishihara, PhD; Katsutoshi Okada, MD; Manami Inoue, MD; Shoichiro Tsugane, MD, for the JPHC Study Group
Soy and isoflavones have been proposed to reduce the risk of cardiovascular risk factors, but their potential as preventatives for cardiovascular disease remains uncertain. We investigated the association of soy and isoflavone intake with risk of cerebral and myocardial infarctions (CI and MI).
To examine the association of soy and isoflavone intake with the risk of CI and MI, we studied 40 462 Japanese (40 to 59 years old, without cardiovascular disease or cancer at baseline). They completed a food-frequency questionnaire (1990–1992) and received follow-up to 2002. After 503 998 person-years of follow-up, we documented incidence of CI (n=587) and MI (n=308) and of mortality for CI and MI combined (n=232). For women, the multivariable hazard ratios and 95% confidence limits for soy intake 5 times per week versus 0 to 2 times per week were 0.64 (0.43 to 0.95) for risk of CI, 0.55 (0.26 to 1.09) for risk of MI, and 0.31 (0.13 to 0.74) for cardiovascular disease mortality. Similar but weaker inverse associations were observed between intake of miso soup and beans and risk of cardiovascular disease mortality. The multivariable hazard ratios for the highest versus the lowest quintiles of isoflavones in women were 0.35 (0.21 to 0.59) for CI, 0.37 (0.14 to 0.98) for MI, and 0.87 (0.29 to 2.52) for cardiovascular disease mortality. An inverse association between isoflavone intake and risk of CI and MI was observed primarily among postmenopausal women. No significant association of dietary intake of soy, miso soup, and beans and isoflavones with CI or MI was present in men.
High isoflavone intake was associated with reduced risk of CI and MI in Japanese women. The risk reduction was pronounced for postmenopausal women.
Circulation. 2007;116:2553-2562.
© 2007 American Heart Association, Inc.
Yoshihiro Kokubo, MD; Hiroyasu Iso, MD; Junko Ishihara, PhD; Katsutoshi Okada, MD; Manami Inoue, MD; Shoichiro Tsugane, MD, for the JPHC Study Group
Soy and isoflavones have been proposed to reduce the risk of cardiovascular risk factors, but their potential as preventatives for cardiovascular disease remains uncertain. We investigated the association of soy and isoflavone intake with risk of cerebral and myocardial infarctions (CI and MI).
To examine the association of soy and isoflavone intake with the risk of CI and MI, we studied 40 462 Japanese (40 to 59 years old, without cardiovascular disease or cancer at baseline). They completed a food-frequency questionnaire (1990–1992) and received follow-up to 2002. After 503 998 person-years of follow-up, we documented incidence of CI (n=587) and MI (n=308) and of mortality for CI and MI combined (n=232). For women, the multivariable hazard ratios and 95% confidence limits for soy intake 5 times per week versus 0 to 2 times per week were 0.64 (0.43 to 0.95) for risk of CI, 0.55 (0.26 to 1.09) for risk of MI, and 0.31 (0.13 to 0.74) for cardiovascular disease mortality. Similar but weaker inverse associations were observed between intake of miso soup and beans and risk of cardiovascular disease mortality. The multivariable hazard ratios for the highest versus the lowest quintiles of isoflavones in women were 0.35 (0.21 to 0.59) for CI, 0.37 (0.14 to 0.98) for MI, and 0.87 (0.29 to 2.52) for cardiovascular disease mortality. An inverse association between isoflavone intake and risk of CI and MI was observed primarily among postmenopausal women. No significant association of dietary intake of soy, miso soup, and beans and isoflavones with CI or MI was present in men.
High isoflavone intake was associated with reduced risk of CI and MI in Japanese women. The risk reduction was pronounced for postmenopausal women.
Circulation. 2007;116:2553-2562.
© 2007 American Heart Association, Inc.
Tuesday, November 13, 2007
Exertion and Acute Aortic Dissection
Role of Exertion or Emotion as Inciting Events for Acute Aortic Dissection
Ioannis S. Hatzaras MD, Jesse E. Bible MD, George J. Koullias MD, Maryann Tranquilli RN, Mansher Singh MD and John A. Elefteriades MD
Section of Cardiothoracic Surgery, Yale University School of Medicine, New Haven, Connecticut.
It is well known that hypertension, aortic dilatation, and collagen disorders predispose to acute aortic dissection (AAD). The inciting events that precede the instant of AAD are incompletely understood.
One hundred seventy-five consecutive patients having AAD, treated at our institution during a 10-year period, were reviewed; 65 were women and 110 were men (mean age 61 years). The ascending aorta was affected in 110 patients, and the descending in 65. Information was collected using patients’ charts supplemented with direct telephone interviews. Ninety patients were contacted; 65 (24 women, 41 men, mean age 61 years, average aortic size 5.56 cm) could recall specific inciting events for their dissection. In 34 patients, the ascending aorta was involved and in 31 the descending. Eighteen patients (28%) had a positive family history of aortic disease, defined as having ≥1 first-degree relative with aortic disease (aneurysm or dissection). In 24 of the 90 patients contacted (27%), strenuous activity was identified as a clear precipitating factor before the acute onset of thoracic pain; in 36 of 90 (40%) severe emotional stress preceded the onset of dissection pain. Three dissections were iatrogenic. Two additional patients reported a severe exacerbation of chronic obstructive pulmonary disease before their acute onset of chest pain.
In conclusion, severe physical and emotional stress may precipitate AAD, presumably on the basis of a transient, severe hypertensive reaction.
The American Journal of Cardiology
Volume 100, Issue 9, 1 November 2007, Pages 1470-1472
Ioannis S. Hatzaras MD, Jesse E. Bible MD, George J. Koullias MD, Maryann Tranquilli RN, Mansher Singh MD and John A. Elefteriades MD
Section of Cardiothoracic Surgery, Yale University School of Medicine, New Haven, Connecticut.
It is well known that hypertension, aortic dilatation, and collagen disorders predispose to acute aortic dissection (AAD). The inciting events that precede the instant of AAD are incompletely understood.
One hundred seventy-five consecutive patients having AAD, treated at our institution during a 10-year period, were reviewed; 65 were women and 110 were men (mean age 61 years). The ascending aorta was affected in 110 patients, and the descending in 65. Information was collected using patients’ charts supplemented with direct telephone interviews. Ninety patients were contacted; 65 (24 women, 41 men, mean age 61 years, average aortic size 5.56 cm) could recall specific inciting events for their dissection. In 34 patients, the ascending aorta was involved and in 31 the descending. Eighteen patients (28%) had a positive family history of aortic disease, defined as having ≥1 first-degree relative with aortic disease (aneurysm or dissection). In 24 of the 90 patients contacted (27%), strenuous activity was identified as a clear precipitating factor before the acute onset of thoracic pain; in 36 of 90 (40%) severe emotional stress preceded the onset of dissection pain. Three dissections were iatrogenic. Two additional patients reported a severe exacerbation of chronic obstructive pulmonary disease before their acute onset of chest pain.
In conclusion, severe physical and emotional stress may precipitate AAD, presumably on the basis of a transient, severe hypertensive reaction.
The American Journal of Cardiology
Volume 100, Issue 9, 1 November 2007, Pages 1470-1472
Losartan decreased myocardial ischemia
Effect of Losartan in Treatment of Exercise-Induced Myocardial Ischemia
a) Cardiology Division, Fondazione “Salvatore Maugeri,” IRCCS, Scientific Institute of Telese Terme, Telese Terme, Italy; b) Department of Health Sciences, School of Medicine, University of Molise, Molise, Italy; c) Department of Clinical Medicine, Cardiovascular and Immunological Sciences, “Federico II” University of Naples, Naples, Italy.
The American Journal of Cardiology
Volume 100, Issue 10, 15 November 2007, Pages 1517-1521
Giancarlo Longobardi MD (a), Graziamaria Corbi MD, PhD (a, b), Francesco Cacciatore MD (a), Pasquale Abete MD (c), Giuseppe Furgi MD (a), Dino Franco Vitale MD (a), Franco Rengo MD (a, c) and Nicola Ferrara MD (a,b)
a) Cardiology Division, Fondazione “Salvatore Maugeri,” IRCCS, Scientific Institute of Telese Terme, Telese Terme, Italy; b) Department of Health Sciences, School of Medicine, University of Molise, Molise, Italy; c) Department of Clinical Medicine, Cardiovascular and Immunological Sciences, “Federico II” University of Naples, Naples, Italy.
Because no controlled clinical studies are available about the possible role of angiotensin II receptor blockers in preventing effort myocardial ischemia, we evaluated the effect of angiotensin II receptor blocker/losartan in preventing exercise-induced myocardial ischemia in patients with coronary artery disease.
Twenty-four sedentary patients with chronic stable ischemia were prospectively randomized to 28 days (double blind) of losartan 100 mg or losartan placebo in 2 divided doses. In each patient the treatment was crossed over to the alternative regimen (28 days, double blind) after a 1-week placebo period (single blind). At the end of each phase a new exercise stress test was performed. At baseline, systolic blood pressure was significantly decreased after losartan 100 mg compared with losartan placebo. At submaximal exercise, systolic blood pressure and rate–pressure product were lower after losartan 100 mg administration compared with losartan placebo, and these findings remained significant at 1-mm ST depression and at peak exercise. Losartan 100 mg administration versus losartan placebo significantly delayed the time to 1-mm ST-depression onset and decreased ST-segment depression at peak exercise and time to recovery of ST-segment depression. Losartan 100 mg administration compared with losartan placebo was able to significantly increase exercise duration and maximal workload during exercise stress testing.
In conclusion, in our study, losartan decreased electrocardiographic parameters of myocardial ischemia in patients with coronary artery disease, suggesting a possible role of this drug in treatment of patients with effort myocardial ischemia.
Twenty-four sedentary patients with chronic stable ischemia were prospectively randomized to 28 days (double blind) of losartan 100 mg or losartan placebo in 2 divided doses. In each patient the treatment was crossed over to the alternative regimen (28 days, double blind) after a 1-week placebo period (single blind). At the end of each phase a new exercise stress test was performed. At baseline, systolic blood pressure was significantly decreased after losartan 100 mg compared with losartan placebo. At submaximal exercise, systolic blood pressure and rate–pressure product were lower after losartan 100 mg administration compared with losartan placebo, and these findings remained significant at 1-mm ST depression and at peak exercise. Losartan 100 mg administration versus losartan placebo significantly delayed the time to 1-mm ST-depression onset and decreased ST-segment depression at peak exercise and time to recovery of ST-segment depression. Losartan 100 mg administration compared with losartan placebo was able to significantly increase exercise duration and maximal workload during exercise stress testing.
In conclusion, in our study, losartan decreased electrocardiographic parameters of myocardial ischemia in patients with coronary artery disease, suggesting a possible role of this drug in treatment of patients with effort myocardial ischemia.
The American Journal of Cardiology
Volume 100, Issue 10, 15 November 2007, Pages 1517-1521
Thursday, November 8, 2007
Coronary syndromes: Treating depression
Treating depression may improve recovery of heart rate variability following coronary syndromesPatients with depression appear to have an impaired ability to recover their heart rate variability following acute coronary syndromes such as heart attack, a factor that could increase their risk of coronary death, according to a report in the September issue of Archives of General Psychiatry, one of the JAMA/Archives journals. However, patients who are treated with antidepressants or whose mood lifts may experience more of an improvement in heart rate variability than those who are untreated or remain depressed.
Heart rate variability refers to the degree to which the heart rate changes from beat to beat in response to normal impulses. "Low heart rate variability predicts death after myocardial infarction [heart attack]," the authors write as background information in the article. "It is reduced in depressed compared with non-depressed patients after myocardial infarction and has been proposed to be a mediator of the increased mortality associated with depression." In non-depressed patients who have an acute coronary episode, heart rate variability drops and then recovers substantially but not completely during the next few months.
Alexander H. Glassman, M.D., of the Columbia University College of Physicians and Surgeons and the New York State Psychiatric Institute, New York, and colleagues measured heart rate variability in 290 depressed patients an average of three weeks after they were hospitalized for acute coronary syndrome, a term encompassing heart events such as heart attack. The patients were then randomly assigned to take either the antidepressant sertraline or placebo for 24 weeks. After 16 weeks, 258 patients returned for a second heart rate variability reading. The severity of each participants' depression and their clinical response to depression treatment also were measured on previously established scales.
At the beginning of the study, previous episodes of depression were associated with lower heart rate variability. At the 16-week follow-up visit, the depressed patients had recovered their heart rate variability more slowly than expected and some even experienced a decrease. Patients who took sertraline had a 9 percent increase in heart rate variability and patients who took placebo had a 10 percent decrease, compared with the 28 to 33 percent increase in recovery of heart rate variability observed in previous studies of non-depressed patients.
"Both sertraline treatment and symptomatic recovery from depression were associated with increased heart rate variability compared with placebo-treated and non-recovered post-acute coronary syndrome control groups, respectively, but this results primarily from decreased heart rate variability in the comparison groups," the authors write.
The mechanisms behind the relationship between heart rate variability, depression and cardiac death remain unclear, the authors note. "What is clear is that depression is associated with biological changes involving increased heart rate, inflammatory response, plasma norepinephrine, platelet reactivity, decreased heart rate variability and now absent post-acute coronary syndrome heart rate variability recovery, all of which is associated with life-threatening consequences. Understanding why these characteristics so strongly associate with depression is crucial to understanding the nature of depression itself," they conclude.
"From a clinician's point of view, patients with depression after myocardial infarction, especially those with prior episodes, should be both carefully watched and aggressively treated, because they are at an elevated cardiac risk and less likely to get better spontaneously."
Heart rate variability refers to the degree to which the heart rate changes from beat to beat in response to normal impulses. "Low heart rate variability predicts death after myocardial infarction [heart attack]," the authors write as background information in the article. "It is reduced in depressed compared with non-depressed patients after myocardial infarction and has been proposed to be a mediator of the increased mortality associated with depression." In non-depressed patients who have an acute coronary episode, heart rate variability drops and then recovers substantially but not completely during the next few months.
Alexander H. Glassman, M.D., of the Columbia University College of Physicians and Surgeons and the New York State Psychiatric Institute, New York, and colleagues measured heart rate variability in 290 depressed patients an average of three weeks after they were hospitalized for acute coronary syndrome, a term encompassing heart events such as heart attack. The patients were then randomly assigned to take either the antidepressant sertraline or placebo for 24 weeks. After 16 weeks, 258 patients returned for a second heart rate variability reading. The severity of each participants' depression and their clinical response to depression treatment also were measured on previously established scales.
At the beginning of the study, previous episodes of depression were associated with lower heart rate variability. At the 16-week follow-up visit, the depressed patients had recovered their heart rate variability more slowly than expected and some even experienced a decrease. Patients who took sertraline had a 9 percent increase in heart rate variability and patients who took placebo had a 10 percent decrease, compared with the 28 to 33 percent increase in recovery of heart rate variability observed in previous studies of non-depressed patients.
"Both sertraline treatment and symptomatic recovery from depression were associated with increased heart rate variability compared with placebo-treated and non-recovered post-acute coronary syndrome control groups, respectively, but this results primarily from decreased heart rate variability in the comparison groups," the authors write.
The mechanisms behind the relationship between heart rate variability, depression and cardiac death remain unclear, the authors note. "What is clear is that depression is associated with biological changes involving increased heart rate, inflammatory response, plasma norepinephrine, platelet reactivity, decreased heart rate variability and now absent post-acute coronary syndrome heart rate variability recovery, all of which is associated with life-threatening consequences. Understanding why these characteristics so strongly associate with depression is crucial to understanding the nature of depression itself," they conclude.
"From a clinician's point of view, patients with depression after myocardial infarction, especially those with prior episodes, should be both carefully watched and aggressively treated, because they are at an elevated cardiac risk and less likely to get better spontaneously."
September 04, 2007
JAMA and Archives Journals
JAMA and Archives Journals
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