Mean platelet volume is associated with myocardial perfusion defect in diabetic patients

Diabetes mellitus (DM) is considered a coronary artery risk equivalent.1 DM is associated with an increased risk of cardiovascular morbidity and mortality.2,3 DM may cause myocardial perfusion defects involving the main coronary artery and myocardial microvascular circulation. Myocardial perfusion imaging (MPI) is a useful non-invasive tool to determine whether there is a myocardial perfusion defect.4Platelet volume is a marker of platelet activation and function and is measured as mean platelet volume (MPV).5 MPV has become a prognostic factor in coronary heart disease and may eventually be accepted as a parameter of platelet activity.6 MPV is emerging as a new risk factor for vascular complications of DM of which atherothrombosis plays a crucial role.7However, to the best of our knowledge, there have been no reports in the literature to evaluate the relationship between MPV and myocardial perfusion defect using MPI in patients with diabetes. Our aim was to evaluate whether there was a relationship between myocardial perfusion defect using myocardial perfusion scintigraphy and MPV in selected diabetic patients.     

Short-term outcomes after hospital discharge in patients admitted with heart failure in Abeokuta,Nigeria: Data from the Abeokuta Heart Failure Registry

Heart failure (HF) has emerged as a global epidemic in at-risk populations, including those living in high-income countries and, as recently described, in low- to middle-income regions of the world, such as sub-Saharan Africa.11-4 While there are well-established HF registries to capture both the characteristics and health outcomes among those hospitalised with AHF in Europe,5,6 North America,7,8 and the Asia–Pacific region,3,9,10 there are few reports from sub-Saharan Africa.11 This includes Nigeria (the most populous country in the region), where HF has emerged as a potentially large public health problem.1Although there have been many therapeutic gains in the management of chronic HF,12 leading to improved overall survival rates,13 there has been very little parallel success (pending further evaluation of the recently reported RELAX trial14 with regard to AHF). This is particularly important when one considers the high proportion of patients who still require hospitalisation for acute HF, and associated high levels of in-patient case fatality and poor short- to medium-term health outcomes.Given the paucity of data describing health outcomes in unselected patients hospitalised with AHF in Nigeria (and indeed the wider sub-Saharan Africa), we examined short- (30 days) to medium-term outcomes (180 days) in consecutive subjects with AHF recruited into the Abeokuta HF registry over a period of six months. Standardised data collected via the registry were used to both describe the baseline characteristics of the cohort and identify correlates of mortality during the six-month follow up.     

Undiagnosed myopathy before surgery and safe anaesthesia table

Patients with muscle pathology are a challenge for anaesthesiologists because of possible life-threatening general anaesthesia complications. A review of the current medical literature on the issue clearly indicates that increasing awareness by anaesthesiologists in recent years has led to a reduction in the occurrence of adverse events in patients with diagnostically well-defined muscle disease. On the other hand, the current emerging aspect is that the great majority of complications concern subjects with clinically non-overt (silent to mildly symptomatic) and thus undiagnosed myopathy. With a view to improving prevention of possible critical anaesthesia complications in such patients, we present a "Safe Anaesthesia Table", listing both the anaesthetic drugs to be avoided and those considered harmless for myopathic patients, irrespective of age and type of pathology. In addition, a brief outline about the clinical aspects suggestive of a possible muscle pathology is also provided. Using "safe drugs" during routine surgical procedures in subjects with suspected undiagnosed myopathy will enable the anaesthesiologist to avoid delaying surgery, while protecting them from anaesthesia complications. By following this approach the presumed myopathy can be properly investigated after surgery.Key words: anaesthesia complications, undiagnosed myopathy, safe anaesthesia, hyperCKemiaPatients suffering from a variety of Muscle Diseases can experience critical adverse events during and after general anaesthesia. Usually these complications are triggered by volatile anaesthetics or succinylcholine. In some myopathic patients, however, life-threatening side effects may also be precipitated by other agents, namely anticholinesterase and neuroleptic drugs (1-6). All complications can be unpredictably combined and present with different clinical severity. As described in a systematic review by DeVries et al. (7), side effects of anaesthetic drugs currently represent 2% of all in-hospital untoward episodes, the decrease being mainly due to extensive use of total intravenous anaesthesia and reduced administration of succinylcholine (1-4). Nonetheless, in view of the possible fatal outcome, they remain a major concern for anaesthesiologists.Acute rhabdomyolysis with the resultant myoglobinuria is among the most severe anaesthesia-related complications for children and adults with muscle pathology. The syndrome may occur alone or as the culmination of a typical episode of Malignant Hyperthermia (MH). Susceptibility to this life-threatening syndrome is an uncommon pharmacogenetic muscle disorder characterized by altered calcium release from the sarcoplasmic reticulum. Besides rhabdomyolysis and myoglobinuria, the complete clinical manifestation of an MH event includes muscle rigidity, high body temperature, metabolic acidosis, hyperkalaemia, and cardiac arrhythmia. Notably, apart from anaesthesia-related MH episodes, susceptible subjects are basically asymptomatic, even though about half of them present raised serum CK (3, 4, 8). Succinylcholine and volatile anaesthetics may trigger a typical MH crisis also in patients with other genetic disorders, as Central Core Disease, a rare congenital myopathy allelic to MH Susceptibility (2, 3, 5). Acute rhabdomyolysis with myoglobinuria mimicking an MH episode, albeit incompletely, is more frequently described in patients with muscular dystrophy and usually referred to as an MH-like episode (1, 2, 9). These episodes are often complicated by hyperkalaemia and severe cardiac arrhythmia, clinical events that have also been reported for other muscle pathologies, as metabolic muscle disorders, congenital myopathies and channelopathies (3, 10-18).Cardiac and respiratory complications are highly critical side effects potentially experienced by myopathic patients, both during and after general anaesthesia. Their occurrence is directly linked to the frequency of underlying ventilatory muscle pathology and cardiac involvement present in muscular dystrophies and related disorders. Volatile anaesthetics may determine heart complications through a calcium-related cardiodepressive effect and a complex dysrhythmic action. Succinylcholine and other depolarizing agents can induce hyperkalaemia followed by fatal ventricular arrhythmia. Serum potassium may also be increased by anticholinesterase drugs (1, 2, 19).Other critical side effects of anaesthetic agents are characterized by myotonic reactions, muscle spasms and localized or generalized rigidity (1-6). Myotonia and related clinical manifestations are usually caused by depolarizing muscle relaxants, but can also be determined by anticholinesterase drugs (1-4, 18). The latter can also enhance vagal responses that aggravate possible autonomic dysregulation. Myotonic reactions induced by succinylcholine or anticholinesterase drugs are often localized to the masseter muscles, but exacerbation may lead to life-threatening respiratory muscle involvement (18). Jaw muscle stiffness may also result from prolonged masseter contraction without electrical activity (spasm): this sign has to be carefully evaluated because possible onset of generalized rigidity, culminating in an MH episode (1-5). Widespread muscle rigidity, associated with central nervous system-induced hyperthermia, can be determined by neuroleptic drugs (butyrophenones and phenothiazines). Accordingly these substances are currently mostly replaced by propofol and opioids (1-4).There are no available population studies on the prevalence of anaesthesia complications in myopathic subjects. Nonetheless, the extent of the problem is illustrated by recent observations on overall prevalence of genetic myopathies, indicating an index of about 1 case per 2,500 inhabitants (20). This estimate is higher than previous data reviewed by Emery in 1991 (21), likely because of the prolonged life expectancy of myopathic patients, e.g. those with Duchenne Muscular Dystrophy (DMD), and because the clinical diagnosis of pauci- or mildly symptomatic patients has been facilitated by the widespread use of DNA molecular analysis.Nowadays in Italy, as in other Western countries, patients with overt myopathy are usually admitted to surgery with a precise diagnosis. Consequently, thanks to specific preventive measures diffusely adopted by anaesthesiologists, potential anaesthesia-associated side effects seem on the whole to have decreased (2-4, 6, 9, 13, 22-26). On the other hand, analysis of recent reports (5, 6, 11, 15, 17, 25, 27) indicates that complications in patients with undiagnosed myopathy are the emerging aspect of the issue, with particular evidence in the extensive review published by Gurnaney et al. (25) on intra- or post-operative rhabdomyolisis, cardiac arrest and hyperkalaemia in myopathic patients. By examination of 173 references, the Authors focused two remarkable points: 1) the great majority of complications involved subjects with undiagnosed myopathy; 2) nearly all the observations concerned patients with DMD or other dystrophinopathy. They were predominantly pauci- or very mildly symptomatic patients, in whom myopathy had been simply overlooked, and the eventual diagnosis of muscular dystrophy pursued on account of the adverse reaction to anaesthesia. Such a high overall level of undiagnosed myopathy was unexpected. A similar observation, that easily escaped general attention because published in a German- language journal, was also previously reported by Breucking et al. (26). Said investigation on 221 patients with DMD or another dystrophinopathy found that severe anaesthesia-related side effects occurred only in children or adolescents with undiagnosed dystrophinopathy.Minimal to mild symptoms of myopathy may also characterize the clinical phenotype of manifesting carriers of dystrophinopathy or other muscular dystrophy, as calpainopathy or dysferlinopathy (28-30). Due to non-overt symptomatology, these carriers could hypothetically go unrecognized at admission to surgery, with the high-risk of anaesthetic complications similar to those in patients with undiagnosed myopathy. This inference has been confirmed by recent literature which indicates at least two cases of anaesthesia-related critical events in carriers of dystrophinopathy (31, 32). To our knowledge , similar data have not yet been reported for other muscular dystrophies.On the whole, currently available data on muscle disease and related anaesthesia complications suggest that the patients involved are mostly those with Clinicallyunclear, because silent or pauci- to mildly symptomatic, Undiagnosed Myopathy (CU Myopathy). With a view to improving prevention of possible critical anaesthesia complications in such patients, we present a list of anaesthetic drugs considered harmless to them ("Safe Anaesthesia Table"). Essential indications are also provided on clinical aspects suggestive of myopathy.     

Sickle cell trait is not associated with chronic kidney disease in adult Congolese patients: a clinic-based,cross-sectional study

Chronic kidney disease (CKD) and end-stage renal disease (ESRD) are associated with significant cardiovascular (CV) and renal morbidity and mortality rates, with substantial economic burden.1,2 Therefore, early identification of CKD patients at high risk of progression is urgently needed for early and targeted treatment to improve patient care.1-3 Diabetes and hypertension are the primary risk factors for CKD and ESRD but do not fully account for CKD and ESRD risk.1-3 Marked variability in the incidence of CKD suggests that factors other than diabetes and hypertension contribute to its aetiology.4Family studies have suggested a genetic component to the aetiology of CKD and ESRD.5 In African Americans, high-risk common variants in the Apol1/MYH9 locus may explain up to 70% of the differences in ESRD rates between European and African Americans.5 While this finding has great implications for ESRD, the identification of additional risk factors for CKD, including genetic loci in association with estimated glomerular filtration rate (eGFR), may help to advance our understanding of the underpinnings of CKD in African Americans.5 In this era of identifying genetic risk factors for kidney disease, it may be appropriate to revisit one of the most common genetic disorders: sickle cell haemoglobinopathies.5In this regard, sickle cell trait (SCT), present in approximately 7–9% of African Americans, has been reported to be a potential candidate gene.6 However, conflicting reports exist as to whether SCT is a risk factor for the progression of nephropathy.6,7 Haemoglobin S (HbS) was selected for in Africa because of the protection it affords from malarial infection, a scenario similar to the protection from trypanosomal infection provided by heterozygosity for APOL1 nephropathy risk variants.6Whereas APOL1 contributes to risk for nephropathy in an autosomal recessive inheritance pattern, HbS reportedly had a dominant effect on risk, with SCT being associated with ESRD.6 In line with this finding, a few small studies on African Americans reported HbS as an independent risk factor for CKD and ESRD.8 However, other studies using a large sample of African Americans stated that SCT was not independently associated with susceptibility to ESRD in African Americans,6 highlighting the need for further studies in other populations such as those of sub-Saharan Africa where SCT is prevalent.Although SCT is very prevalent in black Africans,9 few studies have been conducted to assess the association between SCT and CKD.10 In Democratic Republic of Congo (DRC), the prevalence of CKD and SCT has been reported to be 12% and 17–24%, respectively.11-13 No study has evaluated the frequency of SCT among CKD patients to assess its association with reduced kidney function. Therefore, the aim of this clinic-based, cross-sectional study was to assess the potential association between SCT and CKD among adult Congolese patients.     

Impact of prehypertension on left ventricular mass and QT dispersion in adult black Nigerians

The heterogeneity of individuals with blood pressure (BP) < 140/90 mmHg in terms of cardiovascular (CV) risk was reported as early as 1939 by Robinson and Brucer.1 BP in the range of 120–139/80–89 mmHg (labelled then as prehypertension) was observed to be associated with high risk of progression to hypertension (HT) and cardiovascular disease (CVD) later in life when compared with BP < 120/80 mm Hg.1The term prehypertension was adopted in May 2003 by the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High blood Pressure (JNC-7) to describe BP range of 120–139/80–89 mmHg.2 The resuscitation of this terminology/concept in JNC-7 was a sequel to the documentation of a higher morbidity in individuals with prehypertension in landmark publications.3-5 Prehypertension (PHT) was defined in JNC-7 not only to emphasise the excess risk associated with BP in this range, but also to focus increased clinical and public health attention on prevention.2,6,7Prevalence rates of PHT among adults in the United States, Ghana and northern Nigeria have been reported to be 31, 40 and 58.7%, respectively.7-9 In most studies, including the ones above, PHT was more prevalent than hypertension.7-9 Though PHT is associated with increased risk of major CV events independently of other CV risk factors,10 most individuals (90%) with PHT have at least one cardiovascular risk factor such as dyslipidaemia, abdominal obesity, hyperinsulinaemia, impaired fasting glucose levels, insulin resistance, a prothrombotic state, tobacco use, endothelial dysfunction, and impaired vascular distensibility.6,7,9,10QT interval dispersion (QTd) (the difference between the longest and the shortest QT intervals on a surface ECG), when excessive, is associated with increased risk of cardiovascular morbidity and mortality in population studies, and many clinical conditions, including hypertension.11,12 This has been related to ventricular electrical instability, providing the necessary substrate for lethal ventricular arrhythmias.12,13 Greater QTd and left ventricular mass have been demonstrated in hypertensive individuals compared with normal individuals.11,13,14Considering the well-established, linear relationship between BP and the risk of cardiovascular events, the CV risk associated with PHT is intermediate between normotension and hypertension.2,03 Hence, electrocardiographic and echocardiographic indices of target-organ damage in PHT may also be intermediate between normotension and hypertension. The aims of this study were: (1) to compare the QTd and indices of left ventricular hypertrophy in adult black normal and prehypertensive subjects, and (2) to evaluate the relationship of QTd with electrocardiographic and echocardiographic indices in these subjects.     

Prevalence of the metabolic syndrome and determination of optimal cut-off values of waist circumference in university employees from Angola

The metabolic syndrome is characterised by the presence of multiple metabolic risk factors for cardiovascular (CV) disease1 and type 2 diabetes mellitus.2 In clinical practice, the metabolic syndrome is diagnosed by combinations of three or more of the following five risk factors: central obesity, elevated blood pressure, glucose intolerance, hypertriglyceridaemia and low high-density lipoprotein cholesterol (HDL-C).3-6Worldwide the prevalence of the metabolic syndrome is increasing and becoming a pandemic, and this increase has been mainly attributed to sedentary lifestyle and obesity.7 However, levels of prevalence may vary greatly according to cut-off points of diagnostic criteria and the ethnic group studied.8In sub-Saharan Africa, the majority of countries are experiencing a rapid demographic and epidemiological transition.9,10 Available information from studies in African populations reported a prevalence of the metabolic syndrome ranging from 0% to as high as about 50% or more, depending on the population setting.11 These data however, are limited to some countries,12-21 since there are no available data for the majority of African countries.Angola is a country in sub-Saharan Africa, which in the last few years has undergone significant political changes, accompanied by a rapid economic growth and increased urbanisation. These changes may imply an increasing prevalence of factors contributing to the metabolic syndrome, such as obesity, insufficient physical activity, dyslipidaemia, high blood pressure and glucose intolerance. However, the prevalence of the metabolic syndrome and which factors contribution more to its occurrence in the Angolan population remain unknown.Despite the efforts of several organisations to regulate the algorithm for a definition of the metabolic syndrome,3-5 there is inconsistency on cut-off levels of waist circumference (WC) for defining the metabolic syndrome in several populations. The International Diabetes Federation (IDF)5 recommended the use of ethnic or country-specific cut-off values of WC for the majority of populations, a recommendation reinforced in the Joint Interim Statement (JIS),7 which tried to define different criteria for a definition of the metabolic syndrome.These cut-off values were defined using different methods. For example, Western countries derived their cut-off values of WC from a correlation with body mass index (BMI),4,22 whereas Asian groups tried to define WC cut-off values yielded by receiver operating characteristics (ROC) curve analyses.23 Due to a lack of specific data from African populations, cut-off points of WC derived from the European population have been recommended,5,7 although emerging data suggest that African-specific cut-off values would be different from the European cut-off points currently recommended by the IDF.18,24,25 Therefore, definition of a more reliable cut-off point for WC is needed to build a consistent tool for diagnosis of the metabolic syndrome in sub-Saharan African populations.The aim of this study was to determine the prevalence of the metabolic syndrome in a sample of Africans from Angola, using either the third report of the National Cholesterol Education Program Adult Treatment Panel (ATP III)4 or the JIS7 criteria. Additionally, this study tried to identify threshold WC levels that best predict other components of the metabolic syndrome.     

Evaluation of left atrial mechanical function and atrial conduction abnormalities in Maras powder (smokeless tobacco) users and smokers

Tobacco use can be classified into smoking and smokeless tobacco. Smokeless tobacco is chewed or is absorbed by the nasal and oral mucosae. A type of smokeless tobacco called Maras powder (MP) is used mostly in the south-eastern region of Turkey, and in many cases users become addicted. It is obtained from a tobacco plant species known as Nicotiana rustica Linn. Nicotine concentrations in the tobacco used to produce MP are eight to 10 times higher than those in tobacco used to produce cigarettes.1 MP and its negative effects on the cardiovascular system have been well studied. MP is consumed in such a way that increase in oxidative stress is inevitable and as a result it accelerates the atherosclerotic process.2,3Cigarette smoke includes nicotine and toxic substances such as carbon monoxide and polycyclic aromatic hydrocarbons.4 Inhalation of these substances predisposes to several different atherosclerotic syndromes,5,6 and is also associated with the occurrence of cardiac arrhythmia.7,8The pathophysiological mechanism of cigarette smoking-induced cardiac arrhythmia is complicated, and the pro-fibrotic effect of nicotine on myocardial tissue with its consequent increased susceptibility to catecholamines, may play a role. Moreover, other components of cigarette smoking, such as carbon monoxide, as well as oxidative stress, are likely to cause the generation of arrhythmias. It is also known that cigarette smoking leads to cardiac autonomic dysfunction,9 and it has been implicated in prolonged QT intervals in healthy individuals.10 However, the nicotine concentration in the blood is more likely to cause the pro-arrhythmic effect of cigarette smoking.7,11 The risk of atrial and ventricular arrhythmia rises due to increased nicotine levels.9-12The prolongation of intra- and inter-atrial electromechanical intervals and the inhomogeneous propagation of sinus impulses are well-known electrophysiological characteristics of atria that are prone to fibrillation.13 Left atrial (LA) volume and LA mechanical function have recently been identified as a potential indicator of cardiac disease and arrhythmias.14,15 Prolongation of atrial electromechanical interval and impaired LA mechanical function are associated with adverse clinical events, including atrial fibrillation, stroke, diastolic dysfunction and left ventricular failure.16,17LA mechanical function and atrial conduction abnormalities have not been investigated in MP users and smokers. Therefore, our study was planned to evaluate whether MP damages intra- and inter-atrial conduction intervals and LA mechanical function as much as cigarette smoking.     

Is the relationship of body mass index to severity of coronary artery disease different from that of waist-to- hip ratio and severity of coronary artery disease? Paradoxical findings

Although obesity has been regarded as an independent risk factor for coronary artery disease (CAD) by the American Heart Association (AHA) and investigators of the Framingham Heart study in the 1980s and 1990s,1-3 this has not been supported by recent clinical trials. Moreover, the positive linear relationships between obesity and CAD, as reported by some studies, were as a result of univariate analysis of their data. However, by using multivariate analysis of these study data, which included other cardiovascular risk factors such as diabetes mellitus (DM), hypertension (HTN) and hyperlipidaemia, this relationship was shown to be dramatically reduced.4,5In the Munster Heart study (PROCAM) and similar studies, the positive relationship between body mass index (BMI) and cardiovascular risk factors, with cardiac mortality, which attributed obesity as an independent risk factor, appeared to be due to the associated cardiovascular risk factors that usually accompany obesity.6-10 In these studies there was also a strong positive correlation between high BMI and other cardiovascular risk factors.However, findings of recent studies in this regard were opposite to those of previous studies. According to their findings, not only was obesity not a risk factor for CAD but it also had a protective effect on the progression of CAD, which is known as the ‘obesity paradox’.11,12 On the other hand, abdominal adiposity has always been associated with increased cardiovascular disease and mortality rate, independent of patients’ weight.13,14This study was designed to evaluate not only the impact of BMI but also waist-to-hip ratio (WHR) on the severity of CAD, based on angiographic findings.     

Prevalence of hypertension in the Gambia and Sierra Leone,western Africa: a cross-sectional study

Hypertension (HTN) is a chronic, slowly progressive disease affecting about one billion people globally and leading to about 7.1 million deaths annually. People of African origin may be particularly susceptible to hypertension.1-3 Defined as a sustained systolic blood pressure (SBP) above 140 mmHg, a diastolic blood pressure (DBP) above 90 mmHg or both, the aetiology of HTN can be classified as primary or secondary. While there is no known cause for primary (essential) HTN, which accounts for 90–95% of cases, the remaining 5–10% of cases is defined as secondary HTN and is caused by other disease conditions, which may affect the renal, circulatory, endocrine or other organ systems.Many factors are associated with, and may contribute to the development and persistence of primary HTN, including obesity, stress, smoking,4 low potassium intake, high sodium (salt) and alcohol intake,5,6 familial and genetic influences,7,8 and low birth weight.9 On the other hand, hyperthyroidism, hypothyroidism and other conditions causing hormonal changes may be associated with primary pulmonary HTN.10,11 Regardless of the cause, the consequences of HTN include renal failure, heart failure, myocardial infarction, pulmonary oedema and stroke.12Given these undesirable outcomes, treatment and prevention have assumed increasing emphasis in the management of HTN. Modification of risk factors can be achieved by reducing body weight and decreasing sugar intake, along with lowering alcohol consumption,13,14 as well as reducing salt intake and increasing potassium intake.15,16 Secondary HTN is managed by treating the underlying cause. Drugs available for the treatment of HTN, whether primary or secondary, include calcium-channel blockers (CCB), angiotensin converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), diuretics, α-blockers and β-blockers.Race and ethnicity may influence pathogenesis, prevalence and treatment of HTN,17 perhaps through genetic influences. As a consequence, HTN remains one of the most common CVDs in Africa and one of the most frequent causes of death in the sub-Saharan African region.18,19 In 2000, the rate of HTN in sub-Saharan Africa was reported to be 26.9% in males and 28.3% in females.20 Low socio-economic status (SES) may additionally play an important role in the high prevalence of HTN in western and sub-Saharan Africa.A cross-sectional survey in Tanzania revealed that treatment rates for HTN were very low, especially among people with low SES.21 Low SES led to inadequate education levels as a factor correlating with a higher blood pressure (BP) in adults and resulted in a low treatment rate for HTN due to monetary issues.22Stress, in addition, was another factor related to HTN prevalence, especially in Africa.23 It has been shown that psychosocial stress affects the L-arginine/nitric oxide (NO) system, with a higher susceptibility in black Africans, which in turn contributes to a higher risk of CVD in those individuals.24Therefore, a multiplicity of factors may be associated with and contributing to a high prevalence of HTN among Africans. The current study was undertaken to determine and quantitate the prevalence of HTN in two countries in western sub-Saharan Africa, namely, the Gambia and Sierra Leone.     

Epidemiological African day for evaluation of patients at risk of venous thrombosis in acute hospital care settings

Acute venous thromboembolism (VTE) is a complication in patients hospitalised for a wide variety of acute medical and surgical conditions.1,2 In developed countries, VTE is the most common preventable cause of death among hospitalised patients. Over the last 30 years, extensive research has demonstrated a high risk of VTE in patients who undergo major surgery or experience severe trauma. Patients hospitalised for acute medical illness have approximately the same level of VTE risk as patients who undergo major general surgery.3-5The benefits of VTE prophylaxis are similar for both medical and moderate-risk surgical patients.6,7 VTE prophylaxis is substantially underused. There is great variation in the use of prophylaxis between countries. Even when prophylaxis is used, it may be used sub-optimally.8-10 Although some surveys and studies suggest that physicians have begun to recognise VTE as a serious health problem and use prophylaxis for at least some high-risk patients, a number of recent studies demonstrate that VTE prophylaxis remains underutilised.11-20     

Simultaneous coronary artery bypass grafting and carotid endarterectomy can be performed with low mortality rates

There is controversy over the best approach for patients with concomitant carotid and coronary artery disease.1 Therapeutic strategies include isolated coronary artery bypass grafting (CABG), staged carotid endarterectomy (CEA) and CABG, reversed staged CEA and CABG, and simultaneous procedures under single anaesthesia.2Although reported experiences over three decades are available, combining CEA with CABG remains to be elucidated.3 Furthermore, risk of cerebrovascular accident (CVA), which is one of the major predictors of prognosis of CABG, has been reported to increase up to 14% in patients with severe carotid artery stenosis (> 80%).4-9Peri-operative neurological events such as stroke after CABG are the major neurological complications, which increase with age.10 The incidence of peri-operative stroke has been well documented at approximately 2% of all cardiac surgeries.11 Despite reduced overall complication rates over the years after CABG, the incidence of stroke remains relatively unchanged.10The aetiology of peri-operative stroke is multi-factorial including hypotension or hypoperfusion-induced reduced brain flow, atherosclerosis due to micro- or macro-embolisation, and intra- or extra-cranial vascular diseases.5 In addition, carotid artery disease is a critical factor; however, it is considered unlikely to be the only culprit for peri-operative strokes.12Although no consensus on the optimal management of patients with concomitant carotid and coronary artery disease has been reached,13 simultaneous CEA and CABG surgery is often associated with low rates of mortality and morbidity.14-17 In this study, we report our experience with simultaneous CEA and CABG surgery in our clinic in the light of data in the literature.     

Diagnostic value of plasma C-type natriuretic peptide levels in determination of the duration of mesenteric ischaemia

Acute mesenteric ischaemia (AMI) causes significant morbidity and mortality if not promptly diagnosed and treated. If medical interventions are delayed, the patient may sustain serious ischaemic injury leading to bowel necrosis, so large segments of bowel may require surgical resection. Often these patients have poor clinical outcomes and suffer from complications such as malnutrition.1,2 Mesenteric ischaemia makes up 0.1% of all hospital admissions.1 Even though technological advances have been made in diagnostic laboratory and imaging techniques, AMI remains fatal in 60% of patients diagnosed with this condition.1,3Scientists have been investigating whether there are specific sensitive biomarkers that may indicate the presence of AMI.2,4 Several endothelial markers have been identified as putative biomarkers that may reveal the severity and duration over which mesenteric ischaemia has been sustained.5 However, markers that are effective enough for use in clinical practice have yet to be identified.Natriuretic peptides, namely atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) function in maintaining fluid and electrolyte balance as well as blood vessel tone. CNP is released by vascular endothelial cells, and this biomarker’s function in influencing vascular tone has been investigated.8,7 It has been hypothesised that CNP is an endothelium-derived hyperpolarising factor (EDHF) that specifically affects the degree of resistance in the mesenteric arteries.8 In this study, we aimed to investigate plasma CNP levels during early and advanced stages of mesenteric ischaemia so as to determine whether CNP levels are a good indicator of severity of AMI in a rat model.     

Prevalence and risk factors for hypertension and association with ethnicity in Nigeria: results from a national survey

Hypertension is increasingly being recognised as an important public health problem in sub-Saharan Africa, with 26.9% of men and 28.4% of women in 2000 being estimated to have hypertension.1 Although lower than the prevalence in high-income countries (37.4% in men and 37.2% in women), in terms of numbers of people affected, the burden of hypertension in low- and middle-income countries is greater due to the large population.1Hypertension has been recognised as a strong independent risk factor for heart disease and stroke and a predictor of premature death and disability from cardiovascular complications.2 It has been reported that 13.5% of deaths and 6% of disability-adjusted life years (DALYs) were attributed to hypertension globally, and for low- and middle income people, these figures were 12.9 and 5.6%, respectively over the period 1990 to 2001.3 Although infectious diseases remain the leading cause of mortality and morbidity in sub-Saharan Africa, the prevalence of cardiovascular disease and hypertension is rising rapidly.4It has been emphasised that urbanisation is a key reason for the increasing rates of hypertension, as evidenced by the higher prevalence of hypertension in urban areas.4-6 Urban lifestyles, characterised by sedentary living, increased salt intake, obesity and stress contribute to these differences.5 With the urban population in sub-Saharan Africa projected to increase, a greater risk of hypertension is anticipated.Studies on the association between ethnicity and hypertension in high-income countries have documented a higher prevalence of hypertension in black ethnic groups compared to white ethnic groups.7-9 Reasons for this association are complex, unclear and much debated, reflecting genetic and biochemical mechanisms, and environmental and socio-economic factors.10,11 There is limited evidence regarding differences in the prevalence of hypertension between ethnic groups within the broader classification of black ethnicity.6,12,13Studies in Nigeria and sub-Saharan Africa have mainly involved specific geographical areas or have focused on sub-groups of the population.5,14 Surveys from Nigeria report prevalence estimates ranging from 20.2 to 36.6%, but all have involved participants with different age ranges.15-18 To plan services for hypertension in Nigeria, it is essential to have accurate prevalence estimates for the whole population and to identify populations at risk.Nigeria, which is the most populous country in sub-Saharan Africa, is home to over 250 different ethnic groups. Nigeria is experiencing rapid urbanisation of the population, which is likely to increase the population at risk for hypertension.19 The present study is one of the largest population-based surveys in the region and is able to provide a nationally representative estimate of hypertension for Nigeria.     

Effects of rosuvastatin on ADMA,rhokinase, NADPH oxidase,caveolin-1, hsp 90 and NFkB levels in a rat model of myocardial ischaemia–reperfusion

Ischaemic heart disease remains among the major causes of morbidity and mortality worldwide. The most common form is reduction in blood flow in the coronary arteries supplying blood to the myocardium due to atherosclerotic plaques or vasospasm.1 After ischaemia, reperfusion of the tissue is of great importance for maintenance of the viability of the ischaemic tissue. However reperfusion may paradoxically lead to some morphological changes, enzyme destruction and even death of the still-viable tissue that may be rescued.2Ischaemia–reperfusion (I/R) injury is the mainstay of myocardial infarction, cerebral ischaemia, stroke, haemorrhagic shock and surgical interventions such as organ transplantation, cardiac surgery, coronary angioplasty and thrombolytic treatment-related pathophysiology.3 Endothelial dysfunction, oxidative stress and inflammation are among the most common mechanisms of I/R injury.4,5Asymmetrical dimethyl arginine (ADMA) is an endogenous nitric oxide synthase (eNOS) inhibitor. Its importance is becoming more recognised and further studies are required to determine its use in clinical diagnosis. Available evidence indicates that oxidative stress leads to changes in the activity of enzymes involved in the production and degradation of ADMA.4,5 High levels of ADMA and low levels of nitric oxide (NO) in the coronary arteries of patients with vasospastic angina have been reported.6In the cardiovascular system, NADPH oxidase accounts for the production of reactive oxygen species (ROS), which is produced not only during I/R injury but also under physiological conditions.7 The pro-oxidative NADPH oxidase is present in the plasma membranes of neutrophils, which are an important source of free radical formation and I/R injury.8 Additionally, the rhokinase pathway, which has an important role in regulation of vascular smooth muscle tone, has been shown to be involved in I/R injury, thus making its inhibition a potential target for limiting I/R injury.9It has been reported that inflammatory NFkB expression increased in the I/R-related infarct area; inflammation was suppressed when NFkB expression was inhibited, and cardiac preservation was provided.10 In this context, caveolin-1 was shown to regulate eNOS activation consistently with other signalling molecules such as hsp 90.11 Interaction of hsp 90 with eNOS increases eNOS activity, and consequently, NO production increases.12,13 Myocardial caveolin-1 content is reported to decrease following ischaemia–reperfusion.14 Caveolin-1 deficiency was noted to aggravate cardiac dysfunction and reduce the survival rate in mice that had experienced myocardial infarction (MI).15Rosuvastatin is a synthetic hydrophilic statin widely used in the treatment of dyslipidaemia, as it increases levels of highdensity lipoprotein (HDL) cholesterol, and reduces low-density lipoprotein (LDL) cholesterol and triglyceride levels. Statins have been reported to have anti-inflammatory, antiproliferative, antithrombotic, anti-atherogenic and antihypertensive effects in addition to their cholesterol-lowering effects.8,16-18 Recent studies indicate that rosuvastatin decreases levels of ADMA in hypercholesterolaemia,19 levels of caveolin,20 and also NFkB levels21 in subaracnoid bleeding.To our knowledge, the effects of rosuvastatin on ADMA, rhokinase, caveolin-1, hsp 90 and NFkB levels are not known in cardiac I/R injury. In this study, we aimed to investigate the influence of rosuvastatin on oxidative stress-related rhokinase, NADPH oxidase, ADMA, caveolin-1 and hsp 90 levels in a rat model of I/R injury.     

Hypertensive retinopathy and its association with cardiovascular,renal and cerebrovascular morbidity in Congolese patients

Hypertension is a major public health problem worldwide and on the African continent.1,2 The disease, once considered to be rare outside Europe and North America, is now a leading cause of disability and mortality in developing countries. Its prevalence is projected to reach 30% worldwide by 2025.2Poor control of hypertension increases the likelihood of complications affecting the cardiovascular and cerebrovascular systems, kidney and retina, often labelled under the term target-organ damage (TOD).1 The development of subclinical TOD, such as left ventricular hypertrophy (LVH), increased intima–media thickness of the large vessels, microalbuminuria following glomerular dysfunction, cognitive decline and hypertensive retinopathy precedes the occurrence of major complications, which include stroke, congestive heart failure and myocardial infarction, renal failure and retinal vascular occlusions.3-5 In the Democratic Republic of Congo (DRC), the prevalence of systemic hypertension has been reported to be over 25%,6,7 whereas hypertension and associated complications account for over 20% of deaths among adults.8Studies have demonstrated that TOD increases cardiovascular risks over that already associated with elevated blood pressure alone. For example, it has been shown that once LVH has developed following long-standing systemic hypertension, it behaves as an independent risk factor and a predictor of both further cardiac complications,9 and other incident vascular events such as ischemic stroke and myocardial infarction.10 Similarly, the presence of cerebrovascular and renal damage may raise cardiovascular risk over that conferred by hypertension itself.11,12In addition, hypertensive retinopathy has long been known as a predictor of systemic morbidity and mortality. Both epidemiological and clinical studies have provided evidence that markers of hypertensive retinopathy are associated with raised blood pressure, systemic vascular diseases, and subclinical cerebrovascular and cardiovascular disease, and predict incident clinical stroke, congestive heart failure and mortality due to cardiovascular complications.13 This association of hypertensive retinopathy with other TOD has also been shown to be independent of blood pressure and other risk factors, which supports the recommendation that retinal vascular changes should be assessed in individuals with systemic hypertension for better extra-ocular TOD risk stratification.13While the number of reports on hypertensive TOD has been on the rise on the African continent, the relationship between hypertensive retinopathy and other TOD has largely remained unexplored. The aim of this study was to examine the association of hypertensive retinopathy with LVH, chronic kidney disease (CKD) and stroke in Congolese patients.     

Vascular calcification is not associated with increased ambulatory central aortic systolic pressure in prevalent dialysis patients

Vascular calcification (VC) is a novel vascular risk factor strongly associated with mortality in dialysis patients.1,2 Although various explanations exist for this association, one mechanism is through alterations in pulse-wave velocity (PWV). Vascular calcification is associated with increased aortic PWV,3 which in turn is associated with raised central aortic systolic pressure (CASP) and reduced coronary perfusion.4,5 As a result, brachial pressure may significantly under- or over-estimate central pressure.6Not surprisingly therefore, central blood pressure parameters have been shown to predict hard cardiovascular endpoints (including mortality) better than concomitant brachial measurements.7-10 Whether vascular calcification is directly linked to central pressures is, however, unknown since there are many determinants of aortic stiffening other than calcification. Furthermore, a primarily damaged and stiff aorta may be the target for secondary deposition of calcium.11CASP can be calculated using applanation tonometry-derived peripheral pulse waveforms and associated software.12 This avoids the obvious disadvantages of invasive central pressure determination. The major disadvantage of standard techniques, however, is the one-dimensional static measurement that is obtained, with no information on ambulatory values or nocturnal dipping status.Loss of normal nocturnal systolic blood pressure dipping is prevalent in chronic kidney disease (CKD) and likely contributes to cardiovascular disease.13 Dipping, which can only be assessed using ambulatory monitoring techniques, correlates better with left ventricular mass index (LVMI) in end-stage renal disease than office-based blood pressure measurement.14,15There have been calls for the routine use of ambulatory blood pressure monitoring (ABPM) in clinical studies of CKD13,16 and indeed, for investigations into the utility of ambulatory CASP in clinical practice.17,18 Combining both ambulatory and central pressure measurements is an attractive strategy, but until recently has not been technically possible.A non-invasive wrist watch-like device, BPro with A-Pulse CASP software (HealthStats, Singapore) was recently approved by the US Food and Drug Administration (FDA: K072593) for the measurement of CASP as well as ambulatory blood pressure. It is a small, wrist watch-like, cuffless monitor which obtains radial pressure waveforms by applanation tonometry. BPro has the ability to measure ambulatory CASP and although not yet commercially available, the manufacturer is able to convert data into ambulatory CASP using the same software.As part of a recently published study on vascular calcification,19 we sought to prospectively evaluate whether the presence of vascular calcification had any relationship with ambulatory CASP in our young CKD-5D cohort using the BPro® radial pulse-wave acquisition device. We also sought to determine the utility of inter-dialytic office brachial and central blood pressure measurements in predicting ambulatory parameters.     

Carbon monoxide poisoning increases Tpeak–Tend dispersion and QTc dispersion

Carbon monoxide (CO) poisoning may cause myocardial toxicity and life-threating cardiac arrhythmias.1-3 Acute coronary syndrome, myocardial injury, myocardial dysfunction, cardiac arrest and various types of arrhythmias have been reported in patients with acute CO poisoning.4 CO binds myocardial myoglobin and reduces myocardial oxygen reserve.5 Previous studies reported that episodes of atrial fibrillation, premature ventricular beats and sinusal tachycardia may be seen in patients with acute CO poisoning.6,7 Recent studies also suggested that risk of atrial and ventricular arrhythmia is increased in CO poisoning, due to prolonged QT_c and QT_c dispersion.2,3,8Ventricular repolarisation can be evaluated by measuring QT interval, corrected QT interval, and QT dispersion. Among these parameters, QT dispersion represents the heterogeneity of ventricular repolarisation and was clearly shown to be associated with ventricular arrhythmia.9 T_peak–T_end (T_pT_e) interval is defined as the interval between the peak point and endpoint of the T wave on surface electrocardiography and is a novel index of transmural dispersion of ventricular repolarisation.10 T_pT_e/QT ratio and T_pT_e/QT_c ratio were used in previous studies as an electrocardiographic index in the evaluation of risk of ventricular arrhythmia.11,12The effect of acute CO poisoning on QT intervals was investigated in a number of studies.2,3,8 However, to the best of our knowledge, T_pT_e interval, T_pT_e dispersion, T_pT_e/QT ratio and T_pT_e/QT_c ratio have not been investigated sufficiently in patients with CO poisoning. In this study, we aimed to investigate the effect of acute CO poisoning on electrocardiographic parameters, which indirectly show ventricular repolarisation heterogeneity. We also investigated the relationship between carboxyhaemoglobin (COHb) levels and these parameters.