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Does Type 1 Diabetes Increase Risk Of Heart Attack

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Type 1 diabetes and cardiovascular disease

  • Francesco Cappuccioii,
  • Stefano Genovese3,
  • Eberhard Standl1,
  • Paul Valensi4 &
  • Antonio Ceriello5

Cardiovascular Diabetology volume 12, Commodity number:156 (2013) Cite this commodity

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Abstract

The presence of cardiovascular disease (CVD) in Type 1 diabetes largely impairs life expectancy. Hyperglycemia leading to an increase in oxidative stress is considered to be the central pathophysiological factor of both micro- and macrovascular complications. In Blazon 1 diabetes, the presence of coronary calcifications is also related to coronary artery affliction. Cardiac autonomic neuropathy, which significantly impairs myocardial function and blood flow, as well enhances cardiac abnormalities. Also hypoglycemic episodes are considered to adversely influence cardiac performance. Intensive insulin therapy has been demonstrated to reduce the occurrence and progression of both micro- and macrovascular complications. This has been evidenced by the Diabetes Command and Complications Trial (DCCT) / Epidemiology of Diabetes Interventions and Complications (EDIC) study. The concept of a metabolic memory emerged based on the results of the study, which established that intensified insulin therapy is the standard of treatment of Type 1 diabetes. Hereafter therapies may also include glucagon-like peptide (GLP)-based treatment therapies. Airplane pilot studies with GLP-one-analogues have been shown to reduce insulin requirements.

Introduction

Over the past 40 years, a reduction in the mortality due to cardiovascular (CV) affliction and coronary heart disease (CHD) past near 70% both in diabetic and not-diabetic patients has been observed [i]. The cause is presumed to be a substantial progress in CV risk factor management and interventional cardiology [1]. Furthermore, in patients with blazon 1 diabetes, a decrease in mortality and a remarkable improvement in life expectancy occurred during the by decades [ii, three]. The comparing of ii subcohorts of the Pittsburgh Epidemiology of Diabetes Complications study based on the period of diabetes diagnosis (1950–1964 vs. 1965–1980) found an increase in life expectancy by approximately 14 years [3]. Nevertheless, the overall risk of CVD for people with type 1 diabetes compared to people without diabetes is increased two- to threefold in men, and three- to fivefold in women. A significant increment in CVD mortality related to increasing HbA1c levels has been reported in blazon 1 diabetes [4].

The aim of this newspaper is to present an overview on epidemiologic and pathophysiologic aspects of the relation between type 1 diabetes and CVD. In improver, the management of risk factors, both with view on diagnostic and therapeutic approaches, is addressed.

Epidemiology

In the EURODIAB IDDM Complications Study, including more than 3.200 patients with type 1 diabetes from 16 European countries, the prevalence of CVD was reported to be nine% in men and x% in women, respectively [5]. Related to an increase in duration of diabetes and historic period, an increment from 6% in the age group of fifteen–29 years to 25% in the historic period grouping of 45–59 years, has been observed [v].

In type 1 diabetes every bit compared to type ii diabetes, the human relationship of hyperglycemia with microangiopathy also as macroangiopathy seems to exist more than significant [vi, 7]. According to the results of a large Finnish database, CVD mortality in patients with type 1 diabetes aged from 45–64 years at baseline increases by about l% with every 1% increment of glycated haemoglobin (HbA1c) [six].

In a population-based cohort of 879 individuals with type 1 diabetes from Wisconsin, hyperglycemia was associated with all-cause and cardiovascular mortality [8]. At baseline examination (1980–1982), patients were free of cardiovascular affliction and end-phase renal disease. The patients were followed up until December 2001. The multivariable relative risks comparing the highest quartile of HbA1c (≥12.1%) with the lowest quartile (≤9.4%) were 2.42 (95% CI: 1.54, 3.82; p-trend = 0.0006) for all-cause mortality and iii.28 (95% CI: 1.77, six.08; p-trend < 0.0001) for cardiovascular mortality [8]. This association was nowadays among both sexes, and contained of duration of diabetes, smoking, hypertension, and proteinuria. The relation persisted in subgroup analyses by categories of diabetes duration, smoking, body mass index, proteinuria, and retinopathy [8].

In a Japanese study, which included type one diabetes, who were diagnosed at an historic period of <xviii years betwixt 1965 and 1979, CVD was identified every bit the leading crusade of death in diabetes of more than 20 years of elapsing [nine].

Recently, the long-term clinical outcomes and survival in patients with both young-onset type 2 and type 1 diabetes with a similar age of diagnosis were evaluated [10]. Every bit compared with type 1, type 2 demonstrated to present to exist associated with a more lethal phenotype and a higher mortality. As well diabetic complications were detected more frequently [10].

Pathophysiology / Etiology

Long-term hyperglycemia, both in type 1 and type 2 diabetes, leads to microvascular and macrovascular complications [11]. Microvascular damage affects particularly the retina, kidneys, both the autonomic and peripheral nervous system, while the heart, encephalon, lower limbs, are affected past both micro- and macrovascular disorders [11].

Oxidative stress

Hyperglycemia-induced overproduction of superoxide by the mitochondrial electron-ship chain is supposed to be the fundamental chemical element in the activation of all other pathways involved in the pathogenesis of diabetic complications (Figure 1) [12, 13]. These include an increase in polyol pathway flux and advanced glycation end production formation, an activation of protein kinase C, and an increase in hexosamine pathway flux. Superoxide overproduction is accompanied by increased nitric oxide generation, due to an endothelial nitric oxide synthase (NOS) and inducible NOS uncoupled country. Thus, the formation of the strong oxidant peroxynitrite is favoured, which in turn is dissentious deoxyribonucleic acid (DNA) [12, 13].

Figure 1
figure 1

Pathogenesis of diabetic complications: Hyperglycemia-induced overproduction of superoxide past the mitochondrial electron-ship concatenation is supposed to exist the fundamental element. By activation of different pathways, the formation of the stiff oxidant peroxynitrite is favoured, which in turn is damaging Deoxyribonucleic acid. Through several intermediate steps, acute endothelial dysfunction, contributing to the genesis of diabetic complications, is triggered [xiii].

Full size image

Due to this Deoxyribonucleic acid harm, a rapid activation of poly(adenosine diphosphate [ADP]-ribose) polymerase occurs, in turn depleting the intracellular concentration of its substrate nicotinamide adenine dinucleotide (NAD+), and slowing the rate of glycolysis, electron send, and adenosintriphosphate (ATP) formation. In addition, the ADP-ribosylation of the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is stimulated. These processes event in acute endothelial dysfunction, which is contributing to the genesis of diabetic complications [12, 13].

Inflammation

Also an increment in inflammatory cytokines is supposed to contribute to plaque instability in patients with diabetes [14]. Several inflammatory markers including C-reactive protein, interleukin (IL)-half dozen, IL-8, tumor necrosis factor (TNF)-α, and endothelin-1 are increased during hypoglycemia. The accumulation of inflammatory cytokines is assumed to cause endothelial injury and abnormalities in coagulation, resulting in increased risk for CV events [14].

Hypercoagulability

The coagulation system is contradistinct due to changes in clotting factor levels and/or activeness. Plasma levels of procoagulant factors are increased while fibrinolytic capacity is decreased [fifteen]. Hyperinsulinemia results in increased hepatic synthesis of prothrombotic factors such as fibrinogen and plasminogen activator inhibitor (PAI)-1, thereby creating a thrombotic milieu. Furthermore, diabetes causes quantitative modifications in clotting factors, including glycation and oxidation which as well increment thrombosis chance [15].

Autonomic neuropathy

Cardiac autonomic neuropathy (CAN) detected past standard tests is a common complexity of blazon 1 diabetes. Tin prevalence is around xx% and increases with age and diabetes elapsing with an about 2% almanac increase [16]. Poor glycemic command is a potent adventure cistron for Tin can equally supported by the EURODIAB study [17]. In the DCCT study intensive insulin treatment reduced the incidence of Can by 53% compared to conventional therapy [eighteen]. In the EDIC report, at the 13th-14th year after DCCT closeout, the prevalence and incidence of CAN remained significantly lower in the quondam intensive than in the old conventional group [19].

Several studies showed the predictive value of Can on mortality [16] and that Tin can is an contained predictor of mortality. Tin was reported to be a predictor of CV morbidity and mortality in blazon 1 diabetes [xx]. Various CV disorders associated with CAN and resulting from vagal damage and sympathetic predominance were shown generally in type 2 diabetes and may account for the poor prognosis related to CAN [16]. Such disorders have been far less studied in patients with blazon i diabetes. In a report on patients with type 1 and type 2 diabetes, the prevalence of hypertension was shown to increment with CAN severity (from 3.6% in the patients without Tin can to 36.iv% in those with severe CAN), and Tin was an independent risk factor for hypertension [21]. This association suggests that vagosympathetic imbalance with a relative sympathetic overdrive may be involved in hypertension. In the Pittsburgh EDC written report, Tin can was associated with increased arterial stiffness 18 years later [22]. There is too strong testify, based on studies in patients with blazon 1 or type two diabetes, that QT interval prolongation is an contained predictor of bloodshed, for all-crusade and for cardiovascular deaths [16].

The residue of the activity of the autonomic nervous system is considered to play a primal office for the performance of the diabetic heart [23]. Advanced single-photon emission computed tomography (SPECT) and positron emission tomography (PET) allow to directly and sensitively assess cardiac sympathetic innervation [24–29], coronary claret period [thirty, 31] and myocardial metabolism [32, 33]. In long-term type ane diabetes, myocardial blood flow response to sympathetic stimulation is significantly dumb.

Scintigraphically, cardiac sympathetic dysinnervation was identified in 77% of newly diagnosed metabolically stabilized type 1 diabetic patients [27]. The design of cardiac sympathetic dysinnervation of newly diagnosed blazon 1 diabetic patients is heterogeneous with a predominant amore of the posterior myocardial region [25, 27]. More recent publications, nevertheless, emphasize that neither impairment of metabolic control nor the presence of CV denervation may exist a prerequisite for the development of dumb vasodilatory reserve. Diastolic dysfunction occurring early on in the form of type 1 diabetes has been reported to exist associated with aberrant cardiac sympathetic office every bit assessed past cardiac sympathetic imaging [34, 35].

Neuronal abnormalities are reported to progress with duration of diabetes [36]. In parallel, defects of cardiac sympathetic innervation are more enhanced in long-term than in newly diagnosed type 1 diabetic patients [25, 27]. In patients with a long diabetes history, heterogeneity of cardiac sympathetic dysinnervation, characterized by a more advanced amore of the posterior myocardium in comparison to the anterior, lateral and septal myocardium has been observed [25]. In studies on modest groups of patients with blazon 1 diabetes, frequent sympathetic dysinnervation and a predominance in the posterior myocardial region [37], and proximal sympathetic hyperinnervation of the heart [38] has been observed with PET.

Immunological factors confronting sympathetic ganglia take been reported to be associated with cardiac sympathetic dysfunction [39–45]. Autoantibodies against sympathetic ganglia accept been establish in xx-35% of type 1 diabetic patients [39, 41, 42]. The presence of autoantibodies against sympathetic ganglia has been shown to be associated with scintigraphically assessed cardiac sympathetic dysfunction [39, 41] and electrocardiogram (ECG)-based abnormalities of eye rate variation [41]. Autoantibodies against sympathetic ganglia seem to be rather specific for cardioneuropathy of type one diabetic patients [41].

Hypoglycemia

Additional hemodynamic changes accept been reported to be associated with hypoglycemia [46]. An increment in eye charge per unit and peripheral systolic blood pressure level every bit well as a reduction in primal blood pressure and peripheral arterial resistance (causing a widening of pulse pressure) has been described. Furthermore, an increase in myocardial contractility, stroke book, and cardiac output has been observed [47]. In healthy people, arteries have been reported to become more rubberband during hypoglycemia with a decline in wall stiffness [46]. In people with a longer history of blazon ane diabetes, however, due to an enhanced arterial wall stiffness, hypoglycemia is followed by a less pronounced fall in central arterial pressure [46, 48]. As a consequence, temporarily a markedly increase in the workload of the heart has to exist assumed [46].

In the ECG, hypoglycemia has been found to elicit ST wave changes with lengthening of the QT interval [49] and cardiac repolarization [50]. Thereby, the risk for arrhythmia is causeless to be increased [46]. Related to hypoglycemia, various aberrant center rhythms, including ventricular tachycardia and atrial fibrillation, take been observed. In conclusion, hypoglycemia has been found to potentially cause aberrant electrical activity in the heart and is assumed to can provoke sudden death [46].

An association betwixt hypoglycemia and sudden death has been deteced by different investigators [51–56]. In line with the hypothesis an dissection study demonstrated, that sudden unexpected deaths were four times more frequent in type one diabetic patients than in nondiabetic people [56].

CV risk

Risk factors for microvascular complications

The run a risk of microvascular complications is influenced by several factors, such as puberty, blood pressure, dyslipidemia, gender, diabetes elapsing, smoking and lifestyle [57–59]. Poor metabolic command was identified as an important gene contributing to microvascular complications [60, 61]. In addition, familial risk factors related to all microvascular complications of type 1 diabetes accept been reported [62]. A report performed in blazon 1 diabetic patients (onset age < thirty years) amidst 6,707 families revealed a significantly increased adventure of retinopathy (odds ratio 9.9; CI 5.6–17.7, P < 0.001), nephropathy (half dozen.2; CI 2.9–13.2, P < 0.001) and neuropathy (2.2; CI 1.0–5.ii; P < 0.05) in type i diabetic siblings of patients diagnosed with those complications [62].

In an analysis of 572 type 1 diabetic participants of the Pittsburgh EDC Report (mean follow-upward: 15 years), baseline HbA1c was an independent take chances factor for fatal CAD, along with duration of diabetes and albuminuria [63]. Baseline lower insulin dose, however, was strongly predictive for non-fatal CAD, as was lower renal function, higher diastolic claret force per unit area, and lipids [63].

In patients with diabetes onset at age 5–14 years, a college risk for complications (retinopathy, nephropathy, and neuropathy) has been found as compared to patients diagnosed either at a very young age or later on puberty [62]. In adolescents with type 1 diabetes, an elevated blood pressure or BMI [64–66], dyslipidemia and smoking [67–69] are associated with an elevated risk of incipient nephropathy, early on retinopathy and peripheral neuropathy.

With the onset of diabetic nephropathy, a dramatic increment in the chance for CAD has to be assumed. After 20 years with diabetes, up to 29% of patients with babyhood-onset of type i diabetes and nephropathy will have CAD compared to simply 2–3% in similar patients without nephropathy [70]. In addition to traditional cardiovascular affliction risk factors, elevated hateful HbA1c and macroalbuminuria are significantly associated with alterations in left ventricular structure and part evaluated past cardiac magnetic resonance imaging (MRI) [71].

In observational studies the relationship between claret force per unit area and the progression of chronic kidney disease (CKD) and incident end-stage renal disease (ESRD) is direct and progressive in diabetes [72]. However, most of the evidence is in blazon 2 diabetes, high blood pressure is a common feature likewise of blazon ane diabetes and an increment in claret pressure level in type 1 diabetes increases the chance of nephropathy [73, 74]. Masked hypertension is not infrequent [72]. In people with type 1 diabetes an increase in systolic blood pressure level, specially at night, precedes the development of microalbiminuria [75]. It has been argued that, unlike in blazon two diabetes, in people with blazon one diabetes hypertension develops often afterward the establishment of microalbuminuria. Hence, monitoring blood pressure throughout the 24 hours in type 1 diabetes may be a useful diagnostic procedure.

In the DCCT/EDIC written report, during a fifteen.8-yr median follow-up, 630 of 1441 participants developed hypertension [76]. Intensive therapy during the DCCT reduced the risk of incident hypertension by 24% during EDIC study follow-up. A college HbA1c level, measured at baseline or during follow-upwardly, was associated with increased take chances for incident hypertension. Older age, male sexual activity, family unit history of hypertension, greater baseline body mass index, weight proceeds, and greater albumin excretion charge per unit were independently associated with increased gamble of hypertension. These data show that hyperglycemia is a risk factor for incident hypertension in type i diabetes and that intensive insulin therapy reduces the long-term adventure of developing hypertension.

In a recently published Brazilian report on approximately 1,300 patients with type 1 diabetes, however, body size and blood pressure were not correlated to lipid levels and glycemic command [77]. Correlation of serum lipids with HbA1c was shown to exist heterogeneous across the spectrum of glycemic command. Several pathophysiological factors were suggested based on the HbA1c-level. These results, therefore, practice not back up a unified explanation for cardiovascular risk in type ane diabetes [77].

Cardiovascular risk markers

As demonstrated in 144 participants of the Pittsburgh EDC Study, pulse wave assay (PWA) may contribute to assessment of CV hazard in patients with blazon 1 diabetes [78]. Arterial stiffness alphabetize, augmentation alphabetize, augmentation pressure, subendocardial viability ratio (serving as an guess of myocardial perfusion), electron axle computed tomography-measured coronary artery calcification (CAC) and ankle-brachial index (ABI) were determined. In the assay of cantankerous-sectional associations, greater augmentation pressure was independently associated with prevalent CAD and estimated myocardial perfusion with low ABI (<0.90) [78].

In the DCCT/EDIC study the stiffness/distensibility of the ascending thoracic aorta was measured with magnetic resonance imaging in 879 patients [79]. After adjusting for gender and cohort, aortic distensibility was lower with increasing age, hateful systolic claret pressure level, LDL cholesterol, and HbA1c measured over an average of 22 years. Patients with macroalbuminuria had 25% lower aortic distensibility compared with those without, and lower distensibility also was associated with greater ratio of left ventricular mass to book. This information stand in favour of strong adverse furnishings of hypertension, chronic hyperglycemia and macroalbuminuria on aortic stiffness in type 1 diabetes.

After xv years additional follow-up in EDIC, left ventricular indices were measured past cardiac magnetic resonance imaging in 1017 of the 1371 members of the DCCT accomplice [fourscore]. Mean DCCT/EDIC HbA1c over time was associated with end diastolic volume, stroke volume, cardiac output, left ventricular mass, LV mass/EDV, and aortic distensibility. These associations persisted afterwards adjustment for CVD adventure factors. Thus, cardiac role and remodeling in the EDIC cohort was associated with prior glycemic exposure (glycemic memory).

As role of the EDIC study, 1229 patients with type 1 diabetes underwent ultrasonography of the internal and common carotid arteries in 1994–1996 and again in 1998–2000 [81]. At yr 1 of the EDIC report, the carotid intima-media thickness (IMT) was similar to that in an age- and sex activity-matched nondiabetic population. After half-dozen years, the IMT was significantly greater in the diabetic patients than in the controls. The hateful IMT progression was significantly less in the group that had received intensive therapy during the DCCT than in the group that had received conventional therapy after adjustment for other chance factors. IMT progression was associated with age, and the EDIC base-line systolic claret force per unit area, smoking, the LDL/HDL ratio, and urinary albumin excretion rate and with the mean HbA1c value during the hateful duration of the DCCT. Thus, intensive therapy during the DCCT resulted in decreased progression of IMT vi years after the end of the trial, which once more stands in favour of the effect of glycemic retentivity.

As found by the x-year follow-upward examination of the Pittsburgh Epidemiology of Diabetes Complications (EDC) Study accomplice, CAC is related to clinical coronary artery disease (CAD) independent of other risk factors [82]. This clan, however, was stronger in men than in women [82]. In a accomplice of patients with blazon 1 diabetes (aged 22–50 years), progression of CAC, as identified by electron beam computed tomography (EBCT), was strongly associated with suboptimal glycemic control (HbA1c >7.five%) [83].

In a written report assessing CAC with multislice spiral computed tomography (MSCT), most one third of asymptomatic long-term type 1 diabetic patients presented with coronary calcifications [84]. In patients with coronary calcifications, both cardiac autonomic neuropathy and retinopathy were detected more frequently than in those without (64% vs. 29%, p < 0.02; 59% vs. 31%; p < 0.02). Additionally, duration of diabetes was longer in patients with than without coronary calcification [84].

In a small cohort of boyish, not-obese type 1 diabetic patients, an increased carotid intima-media thickness was found to be associated with insulin resistance. A causal relationship, however, cannot be concluded [85]. According to a prospective longitudinal written report in children and adolescents with type 1 diabetes, systolic blood pressure and body mass index are related to carotid intima-media thickness increase. Command of these gamble factors is supposed to contribute to prevention of carotid intima-media thickness progression [86].

In patients with long-term elapsing blazon i diabetes, sexual dysfunction was demonstrated to be independently associated with CVD and to potentially predict CVD [87].

Results on the predictive value of plasminogen activator inhibitor-ane (PAI-1) are inconsistent. One report found PAI-1 levels to be independently related to CAC in younger (< 45 years) patients with type ane diabetes [88]. According to some other assay, neither PAI-ane nor tPA-PAI-one is an independent predictor of CAD [89].

Diagnosis / Screening

In blazon 1 diabetes, hypertension is often the outcome of nephropathy. Claret pressure level measurement at every routine visit is recommended [90]. In well-nigh adult patients with diabetes, a fasting lipid profile at to the lowest degree once a twelvemonth is recommended [ninety]. Depression-take a chance lipid values (LDL cholesterol < 100 mg/dL, HDL > l mg/dL, triglycerides < 150 mg/dL) provided, assessment may be repeated biannually [xc].

In type 1 diabetic patients with diabetes duration ≥ five years, the screening for nephropathy should include an annual assessment of urine albumin excretion [90]. Irrespective of the degree of urine albumin excretion, in all adults with diabetes serum creatinine should be measured at to the lowest degree annually [xc]. The creatinine value is useful for estimation of glomerular filtration rate (GFR) [90]. In children and adolescent patients, annual screening both for nephropathy and retinopathy is recommended to start at age eleven years in instance of ii years diabetes duration and at historic period 9 years with v years duration, respectively [91].

Screening for signs and symptoms of CV autonomic neuropathy should be started v years afterward the diagnosis of type 1 diabetes [16, 90]. CV reflex tests are the gilt standard in clinical autonomic testing. The most widely used tests assessing cardiac parasympathetic function are based on the time-domain heart charge per unit response to deep breathing, Valsalva maneuver, and postural change. Age is a strong modulator of these tests and needs to be considered when interpreting the results. CV sympathetic role is assessed by measuring the blood pressure response to standing [92].

PWA may contribute to assessment of CV hazard in patients with type 1 diabetes [78]. In a study, greater augmentation pressure level was independently associated with prevalent CAD and estimated myocardial perfusion with depression ABI (<0.90) [78]. Screening patients for silent myocardial ischemia is controversial but seems reasonable in very high risk patients, in detail in those with long duration of diabetes and proteinuria or evidence of peripheral avenue affliction, and in those who wish to outset a vigorous do program. Measurement of CAC score may be suggested as a first line investigation, leading to a stress test if the score is higher than 400 [93, 94].

Handling

Gycemic control

Intensive insulin therapy has been strongly demonstrated to reduce the onset also as progression of all diabetes-related microvascular complications [58, 60, 95–98]. The Diabetes Command and Complications Trial (DCCT)/ Epidemiology of Diabetes Interventions and Complications (EDIC) study plant in approximately 1,200 patients with blazon 1 diabetes a relative CVD risk reduction of 40%, adapted for other adventure factors including albuminuria, when comparing intensive vs. standard treatment (mean HbA1c 7.four% vs. 9.1%) for 11 years [58]. In adolescent patients, intensive treatment (HbA1c viii.1%) every bit compared to conventional treatment (HbA1c 9.8%) has been shown to reduce the risk and progression of background retinopathy by 53%, clinical neuropathy by 60%, and microalbuminuria by 54% [lx]. A prolonged effect of early intensive approaches was also seen in a four yr follow-upwardly of intensively treated adolescent blazon 1 diabetic patients [99].

Several studies confirmed the association between poor glycemic command and an increasing risk for nephropathy [100–102], retinopathy [95, 103, 104], and neuropathy [105–109]. A large proportion of patients, nonetheless, fails to achieve glycemic targets [110–112].

GLP-1 based treatment as an add together-on to insulin

Due to their action on insulin secretion and glucose regulation, glucagone-like peptide (GLP)-1 based treatment approaches have been established in the handling of blazon 2 diabetes. Based on in vitro and animate being studies, GLP-1 based drugs take been causeless to additionally may be effective in preserving and even expanding the beta cell mass [113]. In a small study on 15 patients with newly detected type 1 diabetes, the add-on of exenatide at onset of diabetes has been shown to subtract insulin requirement [113]. Three groups of patients accept been formed: group1 (insulin solitary), group 2 (insulin and exenatide), and group 3 (insulin and sitagliptin).

After one year, a decrease in insulin requirement of xvi.7 ± 12.5, 39.8 ± 17.two, 21.2 ± 9.half dozen units in groups ane, two and three respectively (P = 0.0431) was detected. A mean stimulated c peptide secretion of 0.34 ± 0.12, 0.45 ± 0.34, 0.44 ± 0.5 ng/mL was found (P = 0.8656). The maximum percent preservation in c peptide was observed in the patients of group 2 [113]. Of relevance is the evidence that GLP-1 can protect blazon 1 diabetic patients by both acute hyperglycemia or hypoglycaemia induced endothelial dysfunction, oxidative stress and inflammation [114].

Approaches across glycemic command

In dissimilarity to DCCT/EDIC, some trials did not ostend the association between glycemic control and CVD take a chance [115–117]. Discrepancies are suggested to be based on differences between the report populations [118]. With view on prevention and handling of CAD, it is recommended to focus not but on glycemic command [118]. Traditional gamble factors such every bit albuminuria, the metabolic syndrome, and inflammatory markers should also be addressed [118].

International guidelines recommend lowering blood pressure level in diabetes to prevent macro- and micro-vascular outcomes. However, nigh prove from randomized clinical trials refers to type 2 diabetes. A goal of blood pressure <130 and <80 mmHg has been recommended [90, 119]. The most contempo recommendations of the American Diabetes Association (ADA) set a blood pressure goal of <140/ <lxxx mmHg for persons with diabetes and hypertension; lower targets (such as <130 mm Hg) may exist appropriate in patients if the specific target tin exist achieved without an additional burden of treatment [ninety].

Pharmacological therapy in people with diabetes and hypertension should be with a regimen that includes either an angiotensin converting enzyme (ACE)-inhibitor or an angiotensin-receptor blocker (ARB) [90]. Generally, 2 or more than drugs are required to achieve blood pressure targets in diabetics. Preferred combinations are either ACE-inhibitors or ARBs (not together) with a calcium-channel blocker or a diuretic. For the latter, both thiazide [90] and, more recently, thiazide-like diuretics [120] are recommended.

However, more than recent appraisal of the evidence indicates lack of evidence to back up systolic blood pressure targets <130 mmHg and suggests optimal diastolic blood pressure level between lxxx and 85 mmHg [72].

In studies amid patients with diabetes, regular physical activity has been demonstrated to reduce CVD-related and total bloodshed [11]. Early treatment of hypertension has been reported to prevent end-stage kidney affliction in patients with type 1 diabetes [121]. Angiotensin-converting enzyme (ACE) inhibitors have been demonstrated to be effective and condom in in reducing microalbuminuria [122]. In adolescent patients with persistent microalbuminuria, the use of ACE inhibitors [91, 100, 123] or angiotensin Ii receptor blockers [91] is recommended to prevent the progression to macroalbuminuria. Furthermore, in order to reduce progression of microalbuminuria, cessation of smoking is strongly recommended [117, 124, 125].

Lifestyle modification is recommended for the improvement of lipid profile. In diabetic patients with overt CVD, statins should exist added irrespective of lipid levels [xc]. Statin therapy is also recommended in diabetic patients without CVD anile > 40 years and ≥ 1 other CVD run a risk factor (family history of CVD, hypertension, smoking, dyslipidemia, albuminuria) [ninety]. In patients with lower CV take chances, statin therapy should exist considered if LDL cholesterol remains above 100 mg/dL [90]. In diabetic patients without overt CVD, the goal for LDL cholesterol is 100 mg/dL (2.6 mmol/L). In patients with overt CVD, a LDL cholesterol goal of lxx mg/dL (ane.8 mmol/L), using a loftier dose of a statin, may be considered [90].

Discussion / Outlook

Despite of a remarkable comeback in life expectancy, type one diabetic patients are confronted with an increased adventure of CV mortality, an bear witness often underrecognized. Further improvement may base of operations on consequent gamble assessment and direction of take chances factors. Interpretation of CV risk including the role of surrogate markers deserves more than attention in the hereafter. Currently, optimized glycemic control is considered to exist the most promising approach. Contempo research on a small group of patients suggests the add-on of exenatide at onset of diabetes to decrease insulin requirement. These results, notwithstanding, need to be confirmed past further investigation on larger groups of patients.

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Affiliations

  1. Forschergruppe Diabetes e.V., Helmholtz Center Munich, Ingolstaedter Landstrasse 1, 85764, Munich-Neuherberg, Germany

    Oliver Schnell & Eberhard Standl

  2. University of Warwick, Warwick, Uk

    Francesco Cappuccio

  3. Department of Cardiovascular and Metabolic Diseases, Gruppo Multimedica, Sesto San Giovanni, Milan, Italy

    Stefano Genovese

  4. Service d'Endocrinologie-Diabétologie-Nutrition, Hôpital Jean Verdier, Bondy Cedex, France

    Paul Valensi

  5. Insititut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Hospital Clínic Barcelona, Barcelona, Spain

    Antonio Ceriello

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Correspondence to Oliver Schnell.

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The authors declare that they take no competing interests.

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Schnell, O., Cappuccio, F., Genovese, South. et al. Type 1 diabetes and cardiovascular illness. Cardiovasc Diabetol 12, 156 (2013). https://doi.org/10.1186/1475-2840-12-156

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Keywords

  • Blazon 1 diabetes
  • Cardiovascular affliction

Does Type 1 Diabetes Increase Risk Of Heart Attack,

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