Advances in Cardiology最新文献

{"title":"Metabolic disorders associated with obstructive sleep apnea in adults.","authors":"","doi":"10.1159/000325106","DOIUrl":"https://doi.org/10.1159/000325106","url":null,"abstract":"<p><p>The relationship between metabolic disorders and obstructive sleep apnea (OSA) is multidirectional. Obesity is recognized as the strongest risk factor for OSA. It is unknown whether metabolic syndrome and insulin resistance/type 2 diabetes mellitus contribute to the development or aggravation of OSA, although this is likely. Conversely, OSA may be a risk factor for metabolic disorders. Strong evidence suggests that OSA may increase the risk of developing insulin resistance, glucose intolerance and type 2 diabetes mellitus. OSA has also been associated with the development and/or aggravation of obesity, dyslipidemia, metabolic syndrome and nonalcoholic fatty liver disease - a liver manifestation of metabolic syndrome. In addition, metabolic disorders are confounding factors in OSA. Metabolic disorders and OSA share common intermediate pathogenic pathways, including alterations in autonomic nervous system regulation, increased inflammatory activity, and alterations in adipokine levels and endothelial dysfunction, which may be involved in the interplay between these conditions. Overall, this complexity makes it especially difficult to reveal and understand the links between OSA and metabolic and cardiovascular disorders. The International Diabetes Federation has recently published clinical practice recommendations suggesting that OSA patients should be routinely screened for markers of metabolic disturbance and cardiovascular risk, such as waist circumference, blood pressure, and fasting lipid and glucose levels. It also recommends that the possibility of OSA should be considered in the assessment of all patients with type 2 diabetes mellitus and metabolic syndrome.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"46 ","pages":"67-138"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000325106","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30214265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of metabolic syndrome in patients with acute coronary syndrome.","authors":"M. Feinberg, R. Schwartz, S. Behar","doi":"10.1159/0000115191","DOIUrl":"https://doi.org/10.1159/0000115191","url":null,"abstract":"The reported incidence of metabolic syndrome among patients with an acute coronary syndrome varies between 29 and 46%. The standard fasting cut-off levels for glucose and blood pressure cannot be applied on admission in patients with acute coronary syndrome and therefore modified criteria were used to define the metabolic syndrome. Patients with metabolic syndrome and acute coronary syndrome had increased incidence of heart failure, and worse long-term mortality compared to those without metabolic syndrome. However, they had less heart failure than those with known diabetes mellitus. Hyperglycemia as a risk factor for poor outcome is particularly significant in patients with metabolic syndrome. De novo identification of the metabolic syndrome on admission has the potential to improve risk stratification and management of patients with an acute coronary syndrome.","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"45 1","pages":"114-26"},"PeriodicalIF":0.0,"publicationDate":"2008-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64394264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperglycemia and the pathobiology of diabetic complications.","authors":"D. Aronson","doi":"10.1159/0000115118","DOIUrl":"https://doi.org/10.1159/0000115118","url":null,"abstract":"Both type I and type II diabetes are powerful and independent risk factors for coronary artery disease (CAD), stroke, and peripheral arterial disease. Atherosclerosis accounts for virtually 80% of all deaths among diabetic patients. Prolonged exposure to hyperglycemia is now recognized as a major factor in the pathogenesis of diabetic complications, including atherosclerosis. Hyperglycemia induces a large number of alterations at the cellular level of vascular tissue that potentially accelerates the atherosclerotic process. Animal and human studies have elucidated several major mechanisms that encompass most of the pathological alterations observed in the diabetic vasculture. These include: (1) Nonenzymatic glycosylation of proteins and lipids which can interfere with their normal function by disrupting molecular conformation, alter enzymatic activity, reduce degradative capacity, and interfere with receptor recognition. In addition, glycosylated proteins interact with a specific receptor present on all cells relevant to the atherosclerotic process, including monocyte-derived macrophages, endothelial cells, and smooth muscle cells. The interaction of glycosylated proteins with their receptor results in the induction of oxidative stress and proinflammatory responses. (2) Protein kinase C (PKC) activation with subsequent alteration in growth factor expression. (3) Shunting of excess intracellular glucose into the hexosamine pathway leads to O-linked glycosylation of various enzymes with perturbations in normal enzyme function. (4) Hyperglycemia increases oxidative stress through several pathways. A major mechanism appears to be the overproduction of the superoxide anion (O-2 ) by the mitochondrial electron transport chain. (5) Hyperglycemia promotes inflammation through the induction of cytokine secretion by several cell types including monocytes and adipocytes. Importantly, there appears to be a tight pathogenic link between hyperglycemia-induced oxidant stress and other hyperglycemia-dependent mechanisms of vascular damage described above, namely AGEs formation, PKC activation, and increased flux through the hexosamine pathway. For example, hyperglycemia-induced oxidative stress promotes both the formation of advanced glycosylation end products and PKC activation.","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"45 1","pages":"1-16"},"PeriodicalIF":0.0,"publicationDate":"2008-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/0000115118","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64394167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-insulin antidiabetic therapy in cardiac patients: current problems and future prospects.","authors":"E. Fisman, M. Motro, A. Tenenbaum","doi":"10.1159/0000115193","DOIUrl":"https://doi.org/10.1159/0000115193","url":null,"abstract":"Five types of oral antihyperglycemic drugs are currently approved for the treatment of diabetes: biguanides, sulfonylureas, meglitinides, glitazones and alpha-glucosidase inhibitors. We briefly review the cardiovascular effects of the most commonly used antidiabetic drugs in these groups in an attempt to improve knowledge and awareness regarding their influences and potential risks when treating patients with coronary artery disease (CAD). Regarding biguanides, gastrointestinal disturbances such as diarrhea are frequent, and the intestinal absorption of group B vitamins and folate is impaired during chronic therapy. This deficiency may lead to increased plasma homocysteine levels which, in turn, accelerate the progression of vascular disease due to adverse effects on platelets, clotting factors, and endothelium. The existence of a graded association between homocysteine levels and overall mortality in patients with CAD is well established. In addition, metformin may lead to lethal lactic acidosis, especially in patients with clinical conditions that predispose to this complication, such as heart failure or recent myocardial infarction. Sulfonylureas avoid ischemic preconditioning. During myocardial ischemia, they may prevent opening of the ATP-dependent potassium channels, impeding the necessary hyperpolarization that protects the cell by blocking calcium influx. Meglitinides may exert similar effects due to their analogous mechanism of action. During treatment with glitazones, edema has been reported in 5% of patients, and these drugs are contraindicated in diabetics with NYHA class III or IV cardiac status. The long-term effects of alpha-glucosidase inhibitors on morbidity and mortality rates and on diabetic micro- and macrovascular complications is still unknown. Combined sulfonylurea/metformin therapy reveals additive effects on mortality. Four points should be mentioned: (1) the five oral antidiabetic drug groups present proven or potential cardiac hazards; (2) these hazards are not mere 'side effects' but are deeply rooted in the drugs' mechanisms of action; (3) current data indicate that combined glibenclamide/metformin therapy seems to present a special risk and should be avoided in the long-term management of type 2 diabetics with proven CAD, and (4) Non-Insulin Antidiabetic Therapy in Diabetic Cardiac Patients 155 customized antihyperglycemic pharmacological approaches should be investigated for the optimal treatment of diabetic patients with heart disease. New possibilities are represented by incretin mimetic compounds, dipeptidyl peptidase (DPP)-4 inhibitors, inhaled insulin and eventually oral insulin.","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"45 1","pages":"154-70"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64394303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertension and diabetes.","authors":"E. Grossman, F. Messerli","doi":"10.1159/0000115189","DOIUrl":"https://doi.org/10.1159/0000115189","url":null,"abstract":"Both essential hypertension and diabetes mellitus affect the same major target organs. The common denominator of hypertensive/diabetic target organ-disease is the vascular tree. Left ventricular hypertrophy and coronary artery disease are much more common in diabetic hypertensive patients than in patients suffering from hypertension or diabetes alone. The combined presence of hypertension and diabetes concomitantly accelerates the decrease in renal function, the development of diabetic retinopathy and the development of cerebral diseases. Lowering blood pressure to less than 130/80 mm Hg is the primary goal in the management of the hypertensive diabetic patients. Beta-blockers have been reported to adversely affect the overall risk factor profile in the diabetic patient. In contrast, calcium antagonists, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have been reported to be either neutral or beneficial with regard to the overall metabolic risk factor profile. Combination therapy is usually required to achieve blood pressure goal in diabetic patients. The addition of aldosterone antagonists may be beneficial in patients with resistant hypertension and low levels of serum potassium. Aggressive control of blood pressure, cholesterol and glucose levels should be attempted to reduce the cardiovascular risk of diabetic hypertensive patients.","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"93 1","pages":"82-106"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64394252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial dysfunction in normal and abnormal glucose metabolism.","authors":"Ricardo J Esper,&nbsp;Jorge O Vilariño,&nbsp;Rogelio A Machado,&nbsp;Antonio Paragano","doi":"10.1159/000115120","DOIUrl":"https://doi.org/10.1159/000115120","url":null,"abstract":"<p><p>The endothelium is the common target of all cardiovascular risk factors, and functional impairment of the vascular endothelium in response to injury occurs long before the development of visible atherosclerosis. The endothelial cell behaves as a receptor-effector structure which senses different physical or chemical stimuli that occur inside the vessel and, therefore, modifies the vessel shape or releases the necessary products to counteract the effect of the stimulus and maintain homeostasis. The endothelium is capable of producing a large variety of different molecules which act as agonists and antagonists, therefore balancing their effects in opposite directions. When endothelial cells lose their ability to maintain this delicate balance, the conditions are given for the endothelium to be invaded by lipids and leukocytes (monocytes and T lymphocytes). The inflammatory response is incited and fatty streaks appear, the first step in the formation of the atheromatous plaque. If the situation persists, fatty streaks progress and the resultant plaques are exposed to rupture and set the conditions for thrombogenesis and vascular occlusion. Oxidant products are produced as a consequence of normal aerobic metabolism. These molecules are highly reactive with other biological molecules and are referred as reactive oxygen species (ROS). Under normal physiological conditions, ROS production is balanced by an efficient system of antioxidants, molecules that are capable of neutralizing them and thereby preventing oxidant damage. In pathological states, ROS may be present in relative excess. This shift of balance in favor of oxidation, termed 'oxidative stress', may have detrimental effects on cellular and tissue function, and cardiovascular risk factors generate oxidative stress. Both type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetic patients have mostly been described under enhanced oxidative stress, and both conditions are known to be powerful and independent risk factors for coronary heart disease, stroke, and peripheral arterial disease. Hyperglycemia causes glycosylation of proteins and phospholipids, thus increasing intracellular oxidative stress. Nonenzymatic reactive products, glucose-derived Schiff base, and Amadori products form chemically reversible early glycosylation products which subsequently rearrange to form more stable products, some of them long-lived proteins (collagen) which continue undergoing complex series of chemical rearrangements to form advanced glycosylation end products (AGEs). Once formed, AGEs are stable and virtually irreversible. AGEs generate ROS with consequent increased vessel oxidative damage and atherogenesis. The impressive correlation between coronary artery disease and alterations in glucose metabolism has raised the hypothesis that atherosclerosis and diabetes may share common antecedents. Large-vessel atherosclerosis can precede the development of diabetes, suggesting that rather than at","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"45 ","pages":"17-43"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000115120","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27225772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimal management of combined dyslipidemia: what have we behind statins monotherapy?","authors":"Alexander Tenenbaum,&nbsp;Enrique Z Fisman,&nbsp;Michael Motro,&nbsp;Yehuda Adler","doi":"10.1159/000115192","DOIUrl":"https://doi.org/10.1159/000115192","url":null,"abstract":"<p><p>Evidence of the effectiveness of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) within continuum of atherothrombotic conditions and particularly in the treatment and prevention of coronary heart disease (CHD) is well established. Large-scale, randomized, prospective trials involving patients with CHD have shown that statins reduce the clinical consequences of atherosclerosis, including cardiovascular deaths, nonfatal myocardial infarction and stroke, hospitalization for acute coronary syndrome and heart failure, as well as the need for coronary revascularization. Direct testing of varying degrees of low-density lipoprotein (LDL)- cholesterol lowering has now been carried out in 4 large outcomes trials: PROVE IT-TIMI 22, A to Z, TNT and IDEAL. However, the question whether more aggressive LDL-cholesterol lowering by high-dose statins monotherapy is an appropriate strategy is still open: higher doses of statins are more effective mainly for the prevention of the nonfatal cardiovascular events but such doses are associated with an increase in hepatotoxicity, myopathy and concerns regarding noncardiovascular death. Moreover, despite the increasing use of statins, a significant number of coronary events still occur and many such events take place in patients presenting with type 2 diabetes and metabolic syndrome. More and more attention is now being paid to combined atherogenic dyslipidemia which typically presented in patients with type 2 diabetes and metabolic syndrome. This mixed dyslipidemia (or 'lipid quartet') - hypertriglyceridemia, low high-density lipoprotein (HDL)-cholesterol levels, a preponderance of small, dense LDL particles and an accumulation of cholesterol-rich remnant particles - emerged as the greatest 'competitor' of LDL-cholesterol among lipid risk factors for cardiovascular disease. Most recent extensions of the fibrates trials (BIP, HHS, VAHIT and FIELD) give further support to the hypothesis that patients with insulin-resistant syndromes such as diabetes and/or metabolic syndrome might be the ones to derive the most benefit from therapy with fibrates. However, different fibrates may have a somewhat different spectrum of effects. Other lipid-modifying strategies included using of niacin, ezetimibe, bile acid sequestrants, CETP inhibitors and omega-3 fatty acids. Particularly, ezetimibe/statins combinations provide superior lipid-modifying benefits compared Tenenbaum/Fisman/Motro/Adler 128 with any statins monotherapy in patients with atherogenic dyslipidemia. Atherogenic dyslipidemia is associated with increased levels of chylomicrons and their remnants containing 3 main components: apolipoprotein B-48, triglycerides and cholesterol ester of intestinal origin. Reduction in accessibility for one of them (specifically cholesteryl ester lessening due to ezetimibe administration) could lead to a decrease of the entire production of chylomicrons and result in a decrease of the hepatic body triglycerides po","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"45 ","pages":"127-153"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000115192","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27226936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial dysfunction in normal and abnormal glucose metabolism.","authors":"R. Esper, Jorge Vilariño, R. Machado, Antonio J. Paragano","doi":"10.1159/0000115120","DOIUrl":"https://doi.org/10.1159/0000115120","url":null,"abstract":"The endothelium is the common target of all cardiovascular risk factors, and functional impairment of the vascular endothelium in response to injury occurs long before the development of visible atherosclerosis. The endothelial cell behaves as a receptor-effector structure which senses different physical or chemical stimuli that occur inside the vessel and, therefore, modifies the vessel shape or releases the necessary products to counteract the effect of the stimulus and maintain homeostasis. The endothelium is capable of producing a large variety of different molecules which act as agonists and antagonists, therefore balancing their effects in opposite directions. When endothelial cells lose their ability to maintain this delicate balance, the conditions are given for the endothelium to be invaded by lipids and leukocytes (monocytes and T lymphocytes). The inflammatory response is incited and fatty streaks appear, the first step in the formation of the atheromatous plaque. If the situation persists, fatty streaks progress and the resultant plaques are exposed to rupture and set the conditions for thrombogenesis and vascular occlusion. Oxidant products are produced as a consequence of normal aerobic metabolism. These molecules are highly reactive with other biological molecules and are referred as reactive oxygen species (ROS). Under normal physiological conditions, ROS production is balanced by an efficient system of antioxidants, molecules that are capable of neutralizing them and thereby preventing oxidant damage. In pathological states, ROS may be present in relative excess. This shift of balance in favor of oxidation, termed 'oxidative stress', may have detrimental effects on cellular and tissue function, and cardiovascular risk factors generate oxidative stress. Both type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetic patients have mostly been described under enhanced oxidative stress, and both conditions are known to be powerful and independent risk factors for coronary heart disease, stroke, and peripheral arterial disease. Hyperglycemia causes glycosylation of proteins and phospholipids, thus increasing intracellular oxidative stress. Nonenzymatic reactive products, glucose-derived Schiff base, and Amadori products form chemically reversible early glycosylation products which subsequently rearrange to form more stable products, some of them long-lived proteins (collagen) which continue undergoing complex series of chemical rearrangements to form advanced glycosylation end products (AGEs). Once formed, AGEs are stable and virtually irreversible. AGEs generate ROS with consequent increased vessel oxidative damage and atherogenesis. The impressive correlation between coronary artery disease and alterations in glucose metabolism has raised the hypothesis that atherosclerosis and diabetes may share common antecedents. Large-vessel atherosclerosis can precede the development of diabetes, suggesting that rather than atherosc","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"45 1","pages":"17-43"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/0000115120","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64394316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomarkers in cardiovascular diabetology: interleukins and matrixins.","authors":"Enrique Z Fisman,&nbsp;Yehuda Adler,&nbsp;Alexander Tenenbaum","doi":"10.1159/000115187","DOIUrl":"https://doi.org/10.1159/000115187","url":null,"abstract":"<p><p>The impressive correlation between cardiovascular disease and alterations in glucose metabolism has raised the likelihood that atherosclerosis and type 2 diabetes may share common antecedents. Inflammation is emerging as a conceivable etiologic mechanism for both. Interleukins are regulatory proteins with ability to accelerate or inhibit inflammatory processes, and matrixins are prepro enzymes responsible for the timely breakdown of extracellular matrix. Interleukins (ILs) are classified based on their role in diabetes and atherosclerosis, hypothesizing that each interleukin acts on both diseases in the same direction - regardless if harmful, favorable or neutral. They are clustered into three groups: noxious (the 'bad', 8 members), comprising IL-1, IL-2, IL-6, IL-7, IL-8, IL-15, IL-17 and IL-18; protective (the 'good', 5 members), comprising IL-4, IL-10, IL-11, IL-12 and IL-13; and 'aloof' , comprising IL-5, IL-9, IL-14, IL-16 and IL-19 through IL-29 (15 members). Each group presented converging effects on both diseases. IL-3 was reluctant to clustering and IL-30 through 33 were not included due to the scarce available data. It may be seen that (1) favorable effects of a given interleukin on either diabetes or atherosclerosis predicts similar effects on the other; (2) equally, harmful interleukin effects on one disease can be extrapolated to the other, and (3) absence of influence of a given interleukin on one of these diseases forecasts lack of effects on the other. Matrixins seem to present a similar pathophysiological pattern. These facts further support the unifying etiologic theory of diabetes and heart disease, emphasizing the importance of a cardiovascular diabetologic approach to these cytokines for future research. A pharmacologic simultaneous targeting of interleukins and matrixins might provide an effective means to concurrently control both atherosclerosis and diabetes.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"45 ","pages":"44-64"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000115187","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27226931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertension and diabetes.","authors":"Ehud Grossman,&nbsp;Franz H Messerli","doi":"10.1159/000115189","DOIUrl":"https://doi.org/10.1159/000115189","url":null,"abstract":"<p><p>Both essential hypertension and diabetes mellitus affect the same major target organs. The common denominator of hypertensive/diabetic target organ-disease is the vascular tree. Left ventricular hypertrophy and coronary artery disease are much more common in diabetic hypertensive patients than in patients suffering from hypertension or diabetes alone. The combined presence of hypertension and diabetes concomitantly accelerates the decrease in renal function, the development of diabetic retinopathy and the development of cerebral diseases. Lowering blood pressure to less than 130/80 mm Hg is the primary goal in the management of the hypertensive diabetic patients. Beta-blockers have been reported to adversely affect the overall risk factor profile in the diabetic patient. In contrast, calcium antagonists, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have been reported to be either neutral or beneficial with regard to the overall metabolic risk factor profile. Combination therapy is usually required to achieve blood pressure goal in diabetic patients. The addition of aldosterone antagonists may be beneficial in patients with resistant hypertension and low levels of serum potassium. Aggressive control of blood pressure, cholesterol and glucose levels should be attempted to reduce the cardiovascular risk of diabetic hypertensive patients.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"45 ","pages":"82-106"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000115189","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27226933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}