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Biomedical subjects

Jamal S Rana

Publications and source records attributed to Jamal S Rana.

At least 19 recordsLinked to original sources
PubMed2007

Adiposity compared with physical inactivity and risk of type 2 diabetes in women.

OBJECTIVE: The relative contribution of adiposity and physical inactivity to the risk of developing type 2 diabetes remains controversial. RESEARCH DESIGN AND METHODS: We prospectively examined the individual and joint association of obesity and physical activity with the development of type 2 diabetes in 68,907 female nurses who had no history of diabetes, cardiovascular disease, or cancer at baseline. Adiposity was measured by BMI and waist circumference. Physical activity was assessed through average hours of moderate or vigorous exercise and computation of an MET score. RESULTS: We documented 4,030 incident cases of type 2 diabetes during 16 years of follow-up (from 1986 to 2002). In a multivariate model including age, smoking, and other diabetes risk factors, risk of type 2 diabetes increased progressively with increasing BMI (P < 0.001) and waist circumference (P < 0.001) and with decreasing physical activity levels (P < 0.001). In joint analyses of BMI and physical activity, using women who had a healthy weight (BMI < 25 kg/m(2)) and were physically active (exercise > or = 21.8 MET h/week) as the reference group, the relative risks of type 2 diabetes were 16.75 (95% CI 13.99-20.04) for women who were obese (BMI > or = 30 kg/m(2)) and inactive (exercise < 2.1 MET h/week), 10.74 (8.74-13.18) for women who were active but obese, and 2.08 (1.66-2.61) for women who were lean but inactive. In combined analyses of waist circumference and physical activity, both variables were significant predictors of type 2 diabetes, but the association for waist circumference was substantially stronger than that for physical inactivity. CONCLUSIONS: Obesity and physical inactivity independently contribute to the development of type 2 diabetes; however, the magnitude of risk contributed by obesity is much greater than that imparted by lack of physical activity.

Abdomen↗
PubMed2006

Obesity as compared with physical activity in predicting risk of coronary heart disease in women.

BACKGROUND: The comparative importance of physical inactivity and obesity as predictors of coronary heart disease (CHD) risk remains unsettled. METHODS AND RESULTS: We followed 88 393 women, 34 to 59 years of age, in the Nurses' Health Study from 1980 to 2000. These participants did not have cardiovascular disease and cancer at baseline. We documented 2358 incident major CHD events (including nonfatal myocardial infarction and fatal CHD) during 20 years of follow-up, including 889 cases of fatal CHD and 1469 cases of nonfatal myocardial infarction. In a multivariate model adjusting for cardiovascular risk factors, overweight and obesity were significantly associated with increased risk of CHD, whereas increasing levels of physical activity were associated with a graded reduction in CHD risk (P<0.001). In joint analyses of body mass index (BMI) and physical activity in women who had a healthy weight (BMI, 18.5 to 24.9 kg/m2) and were physically active (exercise > or =3.5 h/wk) as the reference group, the relative risks of CHD were 3.44 (95% confidence interval [CI], 2.81 to 4.21) for women who were obese (BMI > or =30 kg/m2) and sedentary (exercise <1 h/wk), 2.48 (95% CI, 1.84 to 3.34) for women who were active but obese, and 1.48 (95% CI, 1.24 to 1.77) for women who had a healthy weight but were sedentary. In combined analyses of waist-hip ratio and physical activity, both waist-hip ratio and physical activity were significant predictors of CHD, and the highest risk was among women in the lowest category of physical activity and the highest tertile of waist-hip ratio (relative risk=3.03; 95% CI, 1.96 to 4.18). Even a modest weight gain (4 to 10 kg) during adulthood was associated with 27% (95% CI, 12% to 45%) increased risk of CHD compared with women with a stable weight after adjusting for physical activity and other cardiovascular risk factors. CONCLUSIONS: Obesity and physical inactivity independently contribute to the development of CHD in women. These data underscore the importance of both maintaining a healthy weight and regular physical activity in preventing CHD.

Adult↗
PubMed2006

Successful implantation of intravenously administered stem cells correlates with severity of inflammation in murine myocarditis.

The present study was designed to determine whether cardiac inflammation is important for the successful homing of stem cells to the heart after intravenous injection in a murine myocarditis model. Male Bagg albino/c mice were infected with encephalomyocarditis virus (EMCV) to produce myocarditis. Subgroups of mice received single injections by tail vein of embryonic stem cells (ESCs) transfected with green fluorescent protein (GFP) as a marker at days 3, 14, or 60 after infection; other subgroups without stem cell injections were killed at each of these time points to assess the degree of inflammation present. The surviving mice were killed at day 90 after virus infection and hemodynamics, gross pathology, histology, and inflammatory cytokine production in the hearts were measured. Our results indicate that myocardial inflammation was most severe and cytokine production highest at day 14 after EMCV inoculation, and in particular, was strongly positive for interleukin 6. Mice receiving intravenous ESC injections on day 14 after EMCV inoculation showed the largest number of GFP-positive cells at the time of death and the greatest functional improvement compared to uninfected controls without inflammation. We conclude that factors released from myocardium during inflammation are important for enhancing the homing, migration, and implantation of systemically infused stem cells.

Animals↗
PubMed2006

Homing of intravenously infused embryonic stem cell-derived cells to injured hearts after myocardial infarction.

OBJECTIVE: The present study was designed to test whether intravenously infused embryonic stem cell-derived cells could translocate to injured myocardium after myocardial infarction and improve cardiac function. METHODS: Cultured embryonic stem cell-derived cells were transfected with green fluorescent protein. Embryonic stem cell-derived cells were administered through the tail vein (approximately 10(7) cells in 1 mL of medium for each rat) every other day for 6 days in 45 rats after myocardial infarction. Six weeks after myocardial infarction and cell infusion, cardiac function, blood flow, and the numeric density of arterioles were measured to test the benefits of cell therapy. An in vitro Transwell assay was performed to evaluate the embryonic stem cell migration. RESULTS: Ventricular function, regional blood flow, and arteriole density were significantly increased in rats receiving intravenously infused embryonic stem cell-derived cells compared with control rats after myocardial infarction. Histologic analysis demonstrated that infused embryonic stem cell-derived cells formed green fluorescent protein-positive grafts in infarcted myocardium. Additionally, positive immunostaining for cardiac troponin I was found in hearts after myocardial infarction receiving embryonic stem cell-derived cell infusion that corresponded to the green fluorescent protein-positive staining. The Transwell migration assay indicated that cultured neonatal rat cardiomyocytes with overexpression of tumor necrosis factor alpha induced greater migration of embryonic stem cells compared with cardiomyocytes without tumor necrosis factor alpha expression. CONCLUSIONS: Our data demonstrate that intravenously infused embryonic stem cell-derived cells homed to the infarcted heart, improved cardiac function, and enhanced regional blood flow at 6 weeks after myocardial infarction. The in vitro migration assay suggested that such a homing mechanism could be associated with locally released cytokines, such as tumor necrosis factor alpha, that are upregulated in the setting of acute myocardial infarction and heart failure.

Animals↗
PubMed2005

Embryonic stem cells cultured in biodegradable scaffold repair infarcted myocardium in mice.

Our previous findings demonstrated that directly injecting embryonic stem cells (ESCs) into ischemic region of the heart improved cardiac function in animals with experimental myocardial infarction (MI). Tissue engineering with stem cells may provide tissue creation and repair. This study was designed to investigate the effectiveness of grafting of ESC-seeded biodegradable patch on infarcted heart. MI in mice was induced by ligation of the left coronary artery. Mouse ESCs were seeded on polyglycolic-acid (PGA) material patches. Three days after culture, an ESC-seeded patch was transplanted on the surface of ischemic and peri-ischemic myocardium. Eight weeks after MI operation and patch transplantation, hemodynamics and cardiac function were evaluated in four (sham-operated, MI, MI + cell-free patch, and MI + ESC-patch) groups of mice. The blood pressure and left ventricular function were significantly reduced in the MI animals. Compared with MI alone and MI + cell-free patch groups, the animals received MI + ESC-seeded patches significantly improved blood pressure and ventricular function. The survival rate of the MI mice grafted with MI + ESC-seeded patches was markedly higher than that in MI alone or MI + cell-free patch animals. GFP-positive tissue was detected in infarcted area with grafting of ESC-seeded patch, which suggests the survivors of ESCs and possible myocardial regeneration. Our data demonstrate that grafting of ESC-seeded bioabsorbable patch can repair infarcted myocardium and improve cardiac function in MI mice. This novel approach of combining stem cells and biodegradable materials may provide a therapeutic modality for repairing injured heart.

Absorbable Implants↗
PubMed2005

Involvement of COX-2 in VEGF-induced angiogenesis via P38 and JNK pathways in vascular endothelial cells.

OBJECTIVE: Cyclooxygenase-2 (COX-2) is induced by hypoxic stimuli and is also involved in the process of angiogenesis. We previously demonstrated that vascular endothelial growth factor (VEGF) is one of the principal factors produced by hypoxic myocytes and is responsible for the induction of COX-2 expression in endothelial cells. Yet the signaling pathways by which VEGF modulates COX-2 gene expression are still less well defined. We therefore examined the regulation of VEGF-induced COX-2 expression by the mitogen-activated protein kinase (MAPK) family in endothelial cells. METHODS AND RESULTS: Human umbilical vascular endothelial cells (HUVECs) were incubated with U0126 (ERK1/2 inhibitor, 10 microM), SB203580 (p38 inhibitor, 20 microM), and SP600125 (JNK inhibitor, 20 microM), as well as the COX-2 selective inhibitor, NS398, for 1 h before treating with VEGF (20 ng/ml). COX-2 expression induced by VEGF at both mRNA and protein levels was significantly inhibited by selective p38 and JNK inhibitors but not by the ERK1/2 inhibitor. The phosphorylation of p38 and JNK kinases was observed as early as 5 min in HUVECs after VEGF stimulation. Furthermore, the biological significance of the COX-2 gene in endothelial cells was examined by over-expressing or knocking down COX-2 gene expression. (3)H-Thymidine incorporation and Matrigel techniques were used to determine cell proliferation and vascular structure formation. VEGF-induced cell proliferation was significantly reduced when HUVECs were either pre-treated with NS398 (21.52+/-3.6%) or transfected with COX-2 siRNA (34.12+/-5.81%). In contrast, in HUVECs with over-expression of COX-2, VEGF-induced cell proliferation was increased 42.56+/-7.69%. Moreover, the formation of vascular structure assayed by Matrigel demonstrated that VEGF-induced vascular structure formation was accelerated in COX-2 over-expressing cells but attenuated in COX-2 siRNA-transfected cells. CONCLUSION: COX-2 plays an important role in VEGF-induced angiogenesis via p38 and JNK kinase activation pathways. These findings suggest that the cardioprotective role of COX-2 may be, at least in part, through its angiogenic activity.

Anthracenes↗
PubMed2005

Increased level of cardiorespiratory fitness blunts the inflammatory response in metabolic syndrome.

OBJECTIVE: The presence of metabolic syndrome is associated with a higher degree of inflammation. We sought to assess whether the higher levels of cardiorespiratory fitness attenuate the levels of inflammation in people with metabolic syndrome. RESEARCH DESIGN AND METHODS: We studied 449 consecutive asymptomatic men (47+/-7 years) who underwent a maximal treadmill exercise test according to the Bruce protocol. Cardiorespiratory fitness was divided into tertiles based on metabolic equivalents (METs). White blood cells (WBC) (x10(9) cells/L) count was used as marker of inflammation. RESULTS: In our study population, 23% of the participants had the metabolic syndrome. The WBC count increased (p < 0.0001 for trend) with increasing number of risk factors for metabolic syndrome; however there was an inverse relationship (p < 0.0001 for trend) with increasing tertiles of fitness (6.47 cells x 10(9) cells/L for lowest tertile and 5.7 x 10(9) cells/L for highest tertile). Multiple linear regression analyses demonstrated that as compared to individuals with no MS risk factor, the WBC count remained significantly higher in men with metabolic syndrome in first tertile (regression coefficient: 1.2, 95% CI 0.4-2.0, p = 0.003) and second tertile (regression coefficient: 0.61, 95% CI 0.4-2.0, p = 0.02) of cardiorespiratory fitness, respectively. However, in the highest tertile of fitness no increase in level of WBC count was observed with increasing metabolic syndrome risk factors. CONCLUSION: Our findings suggest that in people with metabolic syndrome an increased level of physical fitness might exert its beneficial effect via attenuating inflammation.

Adult↗
PubMed2005

Lipoprotein lipase gene polymorphisms and the risk of target vessel revascularization after percutaneous coronary intervention.

OBJECTIVES: We sought to identify polymorphisms in genes that predispose to restenosis. BACKGROUND: Variations in the lipoprotein lipase (LPL) gene have been implicated in a number of pathophysiologic conditions associated with coronary heart disease. The present study examines the impact of polymorphisms in the LPL gene on restenosis (defined by target vessel revascularization [TVR]) in a large patient population undergoing percutaneous coronary intervention (PCI). A mouse model for restenosis was used to further investigate LPL's role in restenosis. METHODS: The GENetic DEterminants of Restenosis (GENDER) project is a multicenter, prospective study design that enrolled 3,104 consecutive patients after successful PCI. These patients were genotyped for four different LPL gene polymorphisms. In apolipoprotein E (ApoE)*3-Leiden transgenic mice, arterial messenger ribonucleic acid (mRNA) was used to assess LPL expression during a cuff-induced restenotic process. RESULTS: Using multivariable analysis, carriers of the 447Ter allele of the LPL enzyme showed a lower risk of TVR compared with 447Ser homozygotes (p = 0.005). In the mouse model, LPL mRNA levels were increased 40-fold compared with control arteries at 6 h after cuff placement. CONCLUSIONS: The LPL C/G polymorphism (Ser447Ter), resulting in a truncation of the two C-terminal amino acids of the mature LPL protein, appears to be an important protective factor for TVR in humans. The role of LPL in this process was further established in a mouse model, where LPL expression was very strongly up-regulated in the target arterial wall, suggesting a contribution of this lipolytic enzyme to restenosis. Possibly, LPL Ser447Ter genotyping may lead to better risk stratification and tailored therapy in the prevention of restenosis after PCI.

Angioplasty, Balloon, Coronary↗
PubMed2005

Longevity of the placebo effect in the therapeutic angiogenesis and laser myocardial revascularization trials in patients with coronary heart disease.

The long-term beneficial effects of placebo therapy were evaluated in angiogenesis and laser myocardial revascularization trials in patients who had end-stage coronary heart disease. Improvements in mean angina class, exercise treadmill time, and quality of life were mostly maintained at 30 +/- 6 months of follow-up. Persistence of effect cannot be used as evidence of efficacy, and double-blinded trials are essential in this patient population.

Aged↗
PubMed2005

Obesity and clinical restenosis after coronary stent placement.

BACKGROUND: Obesity has been associated with improved clinical outcomes after percutaneous coronary intervention--"obesity paradox." METHODS: We studied 6186 patients pooled from 6 major coronary stent clinical trials. Clinical restenosis was defined as target lesion revascularization (TLR) at 1 year. Body mass index was classified according to World Health Organization criteria as underweight (< 18.5 kg/m2), normal weight (18.5-24.9 kg/m2), overweight (25-29.9 kg/m2), obesity class I (30-34.9 kg/m2), and obesity class II/III (> or = 35 kg/m2). Multivariable logistic regression analysis was used to evaluate the effect of obesity class on TLR. RESULTS: Compared with normal-weight patients, there was a trend to more frequent TLR in patients of obesity class II/III (13.6% vs 10.9%, P = .08). After adjustment for previously defined predictors of TLR, other than the obesity-related intermediate states of diabetes and hypertension, obesity class II/III was associated with 1.33-fold (95% CI 1.00-1.78) higher odds of TLR. In an analysis restricted to patients without diabetes or hypertension, obesity class II/III was also associated with significantly higher odds of undergoing TLR (odd ratio [OR] 2.14, 95% CI 1.21-3.77). CONCLUSION: After coronary stenting, the odds of undergoing TLR were higher in patients with obesity class II/III compared with normal-weight patients. The significant association of severe obesity in nondiabetic and normotensive patients suggests that other obesity-associated mechanisms such as insulin resistance and inflammation should be further explored.

Aged↗
PubMed2005

-455G/A polymorphism and preprocedural plasma levels of fibrinogen show no association with the risk of clinical restenosis in patients with coronary stent placement.

The effect of preprocedural fibrinogen levels on in-stent restenosis is largely unknown. The -455G/A polymorphism of the fibrinogen beta-gene is associated with baseline plasma level or acute phase increase of fibrinogen. Therefore, we hypothesized that there is a relationship between this polymorphism and preprocedural fibrinogen level and clinical restenosis at follow-up among patients with coronary stent placement. The GENetic DEterminants of Restenosis (GENDER) project is a multicenter follow-up study that enrolled 3,146 consecutive patients after successful percutaneous coronary intervention. A coronary stent was placed in 2,309 patients. Of these, 2,257 (97.7%) patients were successfully genotyped for the -455G/A polymorphism. Plasma fibrinogen levels were measured at baseline in a subpopulation of 623 stented patients with the von Clauss method and patients were grouped into tertiles according to fibrinogen levels. Primary endpoint was target vessel revascularization (TVR); secondary combined endpoint was defined as death presumably from cardiac causes, MI not attributable to another coronary artery than the target vessel, and TVR. No association was observed between the -455G/A polymorphism and TVR or combined endpoint (p=0.99, p=0.97, respectively). Multivariate regression analysis revealed that the risk of TVR and combined endpoint was not higher for patients in the highest tertile for fibrinogen versus the lowest tertile (RR=0.60, 95% CI: 0.26-1.37 for TVR, RR=0.64, 95% CI: 0.29-1.44 for combined endpoint). In conclusion, the presence of -455G/A polymorphism in the fibrinogen beta-gene and preprocedural fibrinogen level is not associated with an increased risk of TVR or combined endpoint in a patient population with coronary stent placement. Therefore, these parameters are not worthwhile for stratifying patients at risk for restenosis pre-stenting.

Aged↗
PubMed2005

Metabolic syndrome and risk of restenosis in patients undergoing percutaneous coronary intervention.

OBJECTIVE: Patients with metabolic syndrome have increased risk of cardiovascular events. The number of patients with metabolic syndrome is rapidly increasing, and these patients often need revascularization. However, only limited data are available on the effect of metabolic syndrome on restenosis in patients undergoing percutaneous coronary intervention (PCI). RESEARCH DESIGN AND METHODS: To assess the role of metabolic syndrome in the development of restenosis, we performed an analysis in a population of patients from the GENetic DEterminants of Restenosis (GENDER) study. The GENDER project, a multicenter prospective study, included consecutive patients after successful PCI and was designed to study the predictive value of various genetic and other risk factors for subsequent clinical restenosis, defined as target vessel revascularization (TVR) or combined end point of death, myocardial infarction, and TVR. This subpopulation of GENDER consisted of 901 patients, 448 of whom (49.7%) had metabolic syndrome. RESULTS: On multivariable Cox regression analysis, controlling for age, sex, previous myocardial infarction, stent length, current smoking, and statin therapy, there was no association between increased risk of TVR (hazard ratio 1.03 [95% CI 0.68-1.57]) or the combined end point (1.05 [0.71-1.55]) and the presence of metabolic syndrome. CONCLUSIONS: This study demonstrates that metabolic syndrome is not associated with TVR or the combined end point after PCI. Furthermore, accumulating characteristics of metabolic syndrome were neither associated with increased risk of TVR nor with the combined end point. Therefore, PCI has equal beneficial results in patients with or without metabolic syndrome. This is important information in light of the pandemic proportion of metabolic syndrome that the medical community will face.

Angioplasty, Balloon, Coronary↗
PubMed2004

Obesity and the risk of death after acute myocardial infarction.

BACKGROUND: In the general population, obesity is associated with an increased risk of all-cause death. However, the importance of obesity in patients with established coronary heart disease is less well defined. METHODS: As part of the Determinants of Myocardial Infarction Onset Study, we performed a prospective cohort study of 1898 patients hospitalized with confirmed acute myocardial infarction between 1989 and 1994, with a median follow-up of 3.8 years. We assessed all-cause death through December 1995, using the National Death Index. We categorized patients according to WHO criteria for body mass index (BMI). We compared long-term death according to BMI (kg/m2) by using Cox proportional hazards regression. RESULTS: Of the 1898 eligible patients, 607 (32%) were normal weight (18.5 to 24.9 kg/m2), 832 (44%) were overweight (25.0 to 29.9 kg/m2), 331 (17%) were class I obese (30.0 to 34.9 kg/m2), and 128 (7%) were class II or more obese (> or =35.0 kg/m2). A total of 311 patients died during follow-up. After adjustment for potentially confounding risk factors and excluding patients with noncardiac comorbidity, the risk for death appeared to increase linearly, with increasing BMI across all categories (P for trend =.08). The relative risk of death in all obese patients (> or =30 kg/m2) was 1.46, compared with those with normal weight (95% CI, 0.98 to 2.17). CONCLUSIONS: We found that BMI appeared to have a positive, graded relation with post-myocardial infarction death. Whether weight reduction and secondary prevention strategies would reverse this effect in obese population remains to be seen.

Aged↗
PubMed2004

Chronic obstructive pulmonary disease, asthma, and risk of type 2 diabetes in women.

OBJECTIVE: Inflammation plays a key role in chronic obstructive pulmonary disease (COPD) and asthma. Increasing evidence points toward a role of inflammation in the pathogenesis of type 2 diabetes. We wanted to determine the relation of COPD and asthma with the development of type 2 diabetes. RESEARCH DESIGN AND METHODS: The Nurses' Health Study is a prospective cohort study. From 1988-1996, 103,614 female nurses were asked biennially about a physician diagnosis of emphysema, chronic bronchitis, asthma, and diabetes. RESULTS: During 8 years of follow-up, we documented a total of 2,959 new cases of type 2 diabetes. The risk of type 2 diabetes was significantly higher for patients with COPD than those without (multivariate relative risk 1.8, 95% CI 1.1-2.8). By contrast, the risk of type 2 diabetes among asthmatic patients was not increased (1.0, 0.8-1.2). The asthma results remained nonsignificant even when we evaluated diabetes risk by duration of asthma exposure. CONCLUSIONS: Our findings suggest that COPD may be a risk factor for developing type 2 diabetes. Differences in the inflammation and cytokine profile between COPD and asthma might explain why COPD, but not asthma, is associated with increased risk of type 2 diabetes.

Adult↗
PubMed2003

Cardiomyocytes overexpressing TNF-alpha attract migration of embryonic stem cells via activation of p38 and c-Jun amino-terminal kinase.

Tumor necrosis factor-alpha (TNF-alpha) plays an important role in the pathogenesis of myocardial infarction. Stem cells are able to regenerate infarcted myocardium. This study investigated whether TNF-alpha was able to induce migration of embryonic stem cells (ESCs) in vitro. We used a Transwell assay in which neonatal rat cardiomyocytes, with or without transfection of TNF-alpha cDNA, were plated in the lower compartments and mouse ESCs tagged with green fluorescent protein were added to the upper compartments. TNF-alpha level was significantly increased in the medium of the lower compartments seeded with TNF-alpha-transfected cardiomyocytes. Compared with the controls, overexpression of TNF-alpha significantly enhanced migration of ESCs to the lower compartments. This enhancement was attenuated by preincubation of ESCs with the antibody against the type II TNF-alpha receptor (TNF-RII), but not by the antibody against the type I TNF-alpha receptor (TNF-RI). Western blot analysis showed that the phosphorylated protein levels of p38 and c-Jun amino-terminal kinase (JNK) were significantly increased in TNF-alpha-treated ESCs. Inhibition of the activity of p38 or JNK significantly attenuated TNF-alpha-induced ESC migration. Our data demonstrate that excessive TNF-alpha stimulates TNF-RII and enhances migration of ESCs in vitro. Activation of p38 and JNK is required for TNF-alpha-enhanced ESC migration.

Animals↗
PubMed2003

Circadian variation in the onset of myocardial infarction: effect of duration of diabetes.

There are conflicting reports regarding circadian variation in the onset of acute myocardial infarction (MI) among patients with diabetes. We therefore, studied the circadian pattern of the incidence of acute MI in patients (n = 3,882) who were enrolled in the Onset Study stratified by the presence, type, and duration of diabetes. The Onset Study was conducted at 64 U.S. medical centers between August 1989 and September 1996. We used harmonic regression model to evaluate the circadian variation of MI symptom onset in patients with and without diabetes. Subgroup analysis was performed according to the presence, type, and duration of diabetes by the chi(2) test (dividing the day into four 6-h intervals). Patients without diabetes exhibited a prominent morning peak in the incidence of acute MI symptom onset (P < 0.001). In contrast, patients with type 1 diabetes and type 2 diabetes > or =5 years had a marked attenuation of the morning peak. Patients who had type 2 diabetes diagnosed within the previous 5 years had a pattern of onset of acute MI similar to patients without diabetes. Patients with type 1 diabetes and those with type 2 diabetes > or =5 years have an attenuation of the morning peak in acute MI. Inconsistency in observation of such an effect in patients with diabetes in the past may well have been due to difference in the duration of diabetes and thus the variable extent of underlying autonomic dysfunction.

Age of Onset↗