Prevalence of coronary heart disease,left ventricular failure and hypertension in middle-aged,newly diagnosed Type 2 (non-insulin-dependent) diabetic subjects

Summary The prevalence of coronary heart disease, left ventricular failure and hypertension was examined in a representative group of 133 newly diagnosed Type 2 (non-insulin-dependent) diabetic subjects (70 men, 63 women), aged 45 to 64 years, and in a group of 144 randomly selected non-diabetic control subjects (62 men, 82 women) of the same age group. The prevalence of previous myocardial infarction (major Q-QS abnormalities in resting ECG and/or myocardial infarction verified at hospital) was increased 1.7-fold in male (NS) and 4.4-fold in female (p = 0.007) diabetic patients compared with that found in non-diabetic subjects. Chest pain symptoms and ischaemic ECG abnormalities were about twice as common among diabetic than among non-diabetic subjects. The frequency of coronary heart disease defined by chest pain symptoms and ECG abnormalities was 3.5 times higher in male (p = 0.001) and 3.1 times higher in female (p = 0.001) diabetic patients than in the respective non-diabetic subjects. The frequency of current digitalis therapy was increased 3.3-fold in male (p = 0.006) and 3.9-fold in female (p = 0.001) diabetic patients suggesting an increased frequency of left ventricular failure among diabetic subjects. The prevalence of hypertension, based on the elevated blood pressure levels and/or current use of antihypertensive drugs, was increased 1.6–1.7-fold among the diabetic patients.     

Determinants of subclinical diabetic heart disease

Aims/hypothesis Subclinical left ventricular (LV) dysfunction has been shown by tissue Doppler and strain imaging in diabetic patients in the absence of coronary disease or LV hypertrophy, but the prevalence and aetiology of this finding remain unclear. This study sought to identify the prevalence and the determinants of subclinical diabetic heart disease.Methods A group of 219 unselected patients with type 2 diabetes without known cardiac disease underwent resting and stress echocardiography. After exclusion of coronary artery disease or LV hypertrophy, the remaining 120 patients (age 57±10 years, 73 male) were studied with tissue Doppler imaging. Peak systolic strain of each wall and systolic (Sm) and diastolic (Em) velocity of each basal segment were measured from the three apical views and averaged for each patient. Significant subclinical LV dysfunction was identified according to Sm and Em normal ranges adjusted by age and sex. Strain and Em were correlated with clinical, therapeutic, echocardiographic and biochemical variables, and significant independent associations were sought using a multiple linear regression model.Results Significant subclinical LV dysfunction was present in 27% diabetic patients. Myocardial systolic dysfunction by peak strain was independently associated with glycosylated haemoglobin level (p<0.001) and lack of angiotensin-converting enzyme inhibitor treatment (p=0.003). Myocardial diastolic function (Em) was independently predicted by age (p=0.013), hypertension (p=0.001), insulin (p=0.008) and metformin (p=0.01) treatment.Conclusions/interpretation In patients with diabetes mellitus, subclinical LV dysfunction is common and associated with poor diabetic control, advancing age, hypertension and metformin treatment; ACE inhibitor and insulin therapies appear to be protective.     

Incipient Cardiomyopathy in Young Insulin-dependent Diabetic Patients: A Seven-year Prospective Doppler Echocardiographic Study

Two echo-Doppler cardiographic investigations were performed 7 years apart in 17 insulin-dependent diabetic children without hypertension or nephropathy in order to detect early signs of cardiac abnormalities in this group without ischaemic heart disease. Relative to two matched control groups, the patients had reduced increase in left ventricular size (p < 0.01) and stroke volume (p < 0.05). An initially reduced end systolic wall stress and increased fractional shortening (p < 0.003) was normalized during the 7 years. Concomitant with early signs of autonomic neuropathy and aortic stiffening, left ventricular filling changed with increased velocity during atrial contraction (p < 0.01) correlating to the decreased stroke volumes (r = −0.57, p = 0.016). These early changes could suggest left ventricular restriction but could also reflect a changed sympathetic/parasympathetic balance in diabetic children. A reduced left ventricular cavity size and increased atrial ejection has thus been described in these insulin-dependent children without hypertension, nephropathy or evidence for ischaemic heart disease, suggesting the existence of a metabolically-induced cardiomyopathy.     

Nonvalvular atrial fibrillation associated with cardioembolic stroke: the role of hypertensive heart disease

Abstract Epidemiologists have not identified high risk groups nor the entire spectrum of heart disease, especially the subclinical forms underlying nonvalvular atrial fibrillation (NVAF) predisposing to cardioembolic (CE) stroke. We analysed 36 cases of ‘isolated’ NVAF among 106 consecutive cases of CE stroke after excluding cases of AF associated with valvular disease, myocardial infarcts, ischaemic and other cardio-myopathies (34 cases). This revealed echocardiographic left ventricular hypertrophy (LV mass index 136 ± 25 g, vs normal 68 ± 12 g p < 0.001), enlarged left atria (left atrial area 27.4 ± 3.6 cm² vs normal 14.3 ± 1.6 cm²p < 0.001), normal systolic function and formed the largest group associated with CE stroke (34%), mean age 72.6 years – Study Group D. Eighty nine per cent had known or undetected hypertension compared to 60% in matched controls (x²= 8.3 df= 1 p < 0.01), and hypertension remained the predominant risk factor for left ventricular hypertrophy (LVH). Although all had echocardiographic LVH, 60% had neither electrocardiographs LVH nor cardiomegaly on chest X-ray. Hence usual epidemiologic methods may fail to detect these cases. Hypertensive heart disease is known to predispose to left atrial enlargement and AF. Progressive atrial enlargement is associated with increasing risk of embolie stroke. We conclude that NVAF associated with hypertensive heart disease forms a major component of the spectrum of heart disease associated with NVAF predisposing to CE stroke. Detection and treatment of hypertension to prevent or reverse LVH and atrial enlargement should be an important preventive measure.     

Population implications of electrocardiographic left ventricular hypertrophy

Left ventricular (LV) hypertrophy on the electrocardiogram is an ominous harbinger of cardiovascular disease in the general population markedly increasing the risk of coronary heart disease, cardiac failure, stroke and peripheral arterial disease. This contribution to risk exceeds that of the often accompanying hypertension. Once overt coronary disease occurs, electrocardiographic LV hypertrophy also further escalates risk of cardiovascular morbidity and mortality. The risk associated with electrocardiographic LV hypertrophy is particularly great when repolarization abnormality is present. Electrocardiographic LV hypertrophy and silent electrocardiographic myocardial infarction are similar in evolution and prognosis. LV hypertrophy is an important predictor of risk of cardiac failure; the electrocardiographic manifestation of LV hypertrophy predisposes to cardiac failure more than x-ray cardiac enlargement. Electrocardiographic LV hypertrophy heralds the onset of serious cardiovascular disease and premature mortality despite lack of associated symptoms. The serious prognosis of this abnormality warrants vigorous preventive management. More prospective data are needed comparing the prognosis of echocardiographic anatomical hypertrophy with that diagnosed by electrocardiography.     

Relation of left ventricular isovolumic relaxation time and incoordination to transmitral Doppler filling patterns.

OBJECTIVE--To investigate factors during isovolumic relaxation that determine Doppler filling patterns in patients with left ventricular disease, and thus to identify the underlying mechanisms. DESIGN--85 patients (50 ischaemic heart disease, 35 left ventricular hypertrophy due to aortic stenosis) and 26 controls were studied with Doppler and M mode echocardiography and phonocardiography. 16 patients underwent two studies on separate occasions, to find whether changes in isovolumic relaxation time were reflected by a change in the Doppler A/E ratio. SETTING--A tertiary cardiac referral centre. SUBJECTS--Patients referred for assessment of coronary artery disease or aortic stenosis with left ventricular hypertrophy. MAIN OUTCOMES MEASURES--Doppler filling velocities during early (E wave) and late (A wave) diastole and the A/E ratio, acceleration of the E wave, digitised M mode indices of incoordinate relaxation (change in cavity dimension before mitral valve opening and time from minimum dimension to mitral valve opening), isovolumic relaxation time, M mode measures of diastolic function after mitral valve opening (peak rate of posterior wall thinning and peak rate of dimension increase), and left ventricular end diastolic pressure. RESULTS--A/E correlated with age in normal subjects (r = 0.74), to a lesser extent in left ventricular hypertrophy (r = 0.41), but not significantly in ischaemic heart disease. In all patients, isovolumic relaxation time was significantly and negatively correlated with the acceleration of the E wave, showing its fundamental relation to the force responsible for early diastolic filling (r = -0.71 for left ventricular hypertrophy, and -0.74 for ischaemic heart disease, p value < 0.01). In left ventricular hypertrophy and those ischaemic patients without left ventricular dilatation A/E was correlated both with isovolumic relaxation time (r = 0.68 and 0.60 respectively), and with incoordinate relaxation (r = 0.65 and 0.61). In those ischaemic patients with left ventricular dilatation, the influence of incoordination was lost and isovolumic relaxation time became the dominant influence upon A/E (r = 0.82). Weak correlations of end diastolic pressure and RR interval with A/E, became insignificant once isovolumic relaxation time had been taken into account. Isovolumic relaxation time and incoordination together accounted for over 50% of the variance in the A/E ratio in our patients. Isovolumic relaxation time and the A/E ratio were linearly related. Patients with a short isovolumic relaxation time had evidence of considerable diastolic abnormalities, despite a normal Doppler A/E ratio. In the 16 patients who had two echocardiographic studies, changes in the duration of isovolumic relaxation were accompanied by a change in the Doppler A/E ratio. The relation between these two variables, derived from the group as a whole was similar. CONCLUSIONS--The main factors influencing the A/E ratio in patients with left ventricular disease are two distinct properties of isovolumic relaxation--namely the duration and the extent of incoordinate wall motion. Filling pressure and RR interval are not significant independent determinants, but act only through an effect upon isovolumic relaxation time. Age is an important influence in normal people, but this effect is attenuated in left ventricular hypertrophy and lost in ischaemic ventricular disease.     

Brain natriuretic peptide (BNP) and N-terminal-pro BNP in chronic haemodialysed renal failure

Brain natiuretic peptide (BNP) and N-Terminal-pro BNP (NT-proBNP) are biological markers of left ventricular dysfunction. An increase of one of these peptides is commonly observed in patients with chronic renal failure (CRF) undergoing haemodialysis, in the absence of cardiac failure or acute myocardial ischaemia. The interpretation and clinical implications of this finding are not known. This is a problem because cardiovascular disease is the main cause of morbidity and mortality in patients undergoing haemodialysis. In these patients, left ventricular hypertrophy and left ventricular dysfunction were associated with increased mortality. A biological marker of left ventricular dysfunction enabling early identification of high risk patients would be very useful in this population. Chronic renal failure and haemodialysis do not explain increased levels of BNP and NT-proBNP. Expansion of extra-cellular volume causing myocardial stretching and increased left ventricular pressures is the principal cause of increased BNP and NT-proBNP in haemodialysis patients. The left ventricular hypertrophy and endothelial dysfunction in severe chronic renal failure, systolic and diastolic left ventricular dysfunction, the associated cardiac disease (usually ischaemic) also contribute to this increase. In view of the relationship with left ventricular hypertrophy, left ventricular dysfunction, ischaemic heart disease, BNP and NT-proBNP are predictive factors of total and/or cardiovascular mortality in asymptomatic haemodialysed patients. The BNP/NT-proBNP value should allow identification of high risk asymptomatic haemodialysed patients who would benefit from aggressive evaluation of left ventricular hypertrophy and dysfunction and appropriate, targeted therapeutic intervention.     

Relation of left ventricular isovolumic relaxation time and incoordination to transmitral Doppler filling patterns

Objective—To investigate factors during isovolumic relaxation that determine Doppler filling patterns in patients with left ventricular disease, and thus to identify the underlying mechanisms.Design—85 patients (50 ischaemic heart disease, 35 left ventricular hypertrophy due to aortic stenosis) and 26 controls were studied with Doppler and M mode echocardiography and phonocardiography. 16 patients underwent two studies on separate occasions, to find whether changes in isovolumic relaxation time were reflected by a change in the Doppler A/E ratio.Setting—A tertiary cardiac referral centre.Subjects—Patients referred for assessment of coronary artery disease or aorticstenosis with left ventricular hypertrophy.Main outcomes measures—Doppler filling velocities during early (E wave) and late (A wave) diastole and the A/E ratio, acceleration of the E wave, digitised M mode indices of incoordinate relaxation (change in cavity dimension before mitral valve opening and time from minimum dimension to mitral valve opening), isovolumic relaxation time, M mode measures of diastolic function after mitral valve opening (peak rate of posterior wall thinning and peak rate of dimension increase), and left ventricular end diastolic pressure.Results—A/E correlated with age in normal subjects (r = 0·74), to a lesser extent in left ventricular hypertrophy (r = 0·41), but not significantly in ischaemic heart disease. In all patients, isovolumic relaxation time was significantly and negatively correlated with the acceleration of the E wave, showing its fundamental relation to the force responsible for early diastolic filling (r = −0·71 for left ventricular hypertrophy, and −0·74 for ischaemic heart disease, p value < 0·01). In left ventricular hypertrophy and those ischaemic patients without left ventricular dilatation A/E was correlated both with isovolumic relaxation time (r = 0·68 and 0·60 respectively), and with incoordinate relaxation (r = 0·65 and 0·61). In those ischaemic patients with left ventricular dilatation, the influence of incoordination was lost and isovolumic relaxation time became the dominant influence upon A/E (r = 0·82). Weak correlations of end diastolic pressure and RR interval with A/E, became insignificant once isovolumic relaxation time had been taken into account. Isovolumic relaxation time and incoordination together accounted for over 50% of the variance in the A/E ratio in our patients. Isovolumic relaxation time and the A/E ratio were linearly related. Patients with a short isovolumic relaxation time had evidence of considerable diastolic abnormalities, despite a normal Doppler A/E ratio. In the 16 patients who had two echocardiographic studies, changes in the duration of isovolumic relaxation were accompanied by a change in the Doppler A/E ratio. The relation between these two variables, derived from the group as a whole was similar.Conclusions—The main factors influencing the A/E ratio in patients with left ventricular disease are two distinct properties of isovolumic relaxation—namely the duration and the extent of incoordinate wall motion. Filling pressure and RR interval are not significant independent determinants, but act only through an effect upon isovolumic relaxation time. Age is an important influence in normal people, but this effect is attenuated in left ventricular hypertrophy and lost in ischaemic ventricular disease.     

Relation of left ventricular isovolumic relaxation time and incoordination to transmitral Doppler filling patterns

Objective—To investigate factors during isovolumic relaxation that determine Doppler filling patterns in patients with left ventricular disease, and thus to identify the underlying mechanisms.

Design—85 patients (50 ischaemic heart disease, 35 left ventricular hypertrophy due to aortic stenosis) and 26 controls were studied with Doppler and M mode echocardiography and phonocardiography. 16 patients underwent two studies on separate occasions, to find whether changes in isovolumic relaxation time were reflected by a change in the Doppler A/E ratio.

Setting—A tertiary cardiac referral centre.

Subjects—Patients referred for assessment of coronary artery disease or aorticstenosis with left ventricular hypertrophy.

Main outcomes measures—Doppler filling velocities during early (E wave) and late (A wave) diastole and the A/E ratio, acceleration of the E wave, digitised M mode indices of incoordinate relaxation (change in cavity dimension before mitral valve opening and time from minimum dimension to mitral valve opening), isovolumic relaxation time, M mode measures of diastolic function after mitral valve opening (peak rate of posterior wall thinning and peak rate of dimension increase), and left ventricular end diastolic pressure.

Results—A/E correlated with age in normal subjects (r = 0·74), to a lesser extent in left ventricular hypertrophy (r = 0·41), but not significantly in ischaemic heart disease. In all patients, isovolumic relaxation time was significantly and negatively correlated with the acceleration of the E wave, showing its fundamental relation to the force responsible for early diastolic filling (r = −0·71 for left ventricular hypertrophy, and −0·74 for ischaemic heart disease, p value < 0·01). In left ventricular hypertrophy and those ischaemic patients without left ventricular dilatation A/E was correlated both with isovolumic relaxation time (r = 0·68 and 0·60 respectively), and with incoordinate relaxation (r = 0·65 and 0·61). In those ischaemic patients with left ventricular dilatation, the influence of incoordination was lost and isovolumic relaxation time became the dominant influence upon A/E (r = 0·82). Weak correlations of end diastolic pressure and RR interval with A/E, became insignificant once isovolumic relaxation time had been taken into account. Isovolumic relaxation time and incoordination together accounted for over 50% of the variance in the A/E ratio in our patients. Isovolumic relaxation time and the A/E ratio were linearly related. Patients with a short isovolumic relaxation time had evidence of considerable diastolic abnormalities, despite a normal Doppler A/E ratio. In the 16 patients who had two echocardiographic studies, changes in the duration of isovolumic relaxation were accompanied by a change in the Doppler A/E ratio. The relation between these two variables, derived from the group as a whole was similar.

Conclusions—The main factors influencing the A/E ratio in patients with left ventricular disease are two distinct properties of isovolumic relaxation—namely the duration and the extent of incoordinate wall motion. Filling pressure and RR interval are not significant independent determinants, but act only through an effect upon isovolumic relaxation time. Age is an important influence in normal people, but this effect is attenuated in left ventricular hypertrophy and lost in ischaemic ventricular disease.

     

Comprehensive assessment of hypertensive heart disease: cardiac magnetic resonance in focus

Arterial hypertension represents the most frequent cardiovascular risk factor that is associated with cardiac remodeling. Hypertensive heart disease was defined by the presence of left ventricular hypertrophy (LVH) and diastolic dysfunction, and it has been diagnosed by echocardiography in everyday clinical practice. Interstitial myocardial fibrosis is the underlying cause of hypertension-induced cardiac remodeling, and it could not be visualized with different echocardiographic methods. Cardiac magnetic resonance (CMR) and its methods such as late gadolinium enhancement, and T1 mapping provides qualitative and quantitative assessment of interstitial myocardial fibrosis in hypertensive patients. Furthermore, CMR can provide differentiation of LVH between hypertensive patients and cardiomyopathies (hypertrophic or Fabry disease). Timely diagnosis of cardiac impairment and early treatment is essential because regression of LVH could be achieved with adequate treatment. Diffuse cardiac fibrosis in hypertensive patients might be an underlying mechanism that explains the increased cardiovascular morbidity and mortality in this population. Future longitudinal investigations are necessary to determine causal relationship between diffuse fibrosis and cardiovascular outcome in these patients. The aim of this review is to summarize the current knowledge regarding CMR techniques and their potential usage in patients with hypertensive heart disease.

     

Subclinical cardiac dysfunction in acromegaly: evidence for a specific disease of heart muscle

Acromegaly is associated with an increased cardiac morbidity and mortality, but it is not clear whether this is the result of increased incidence of hypertension and coronary heart disease or of a specific disease of heart muscle. Thirty four acromegalic patients were studied by non-invasive techniques. Seven of these patients had raised plasma concentrations of growth hormone at the time of study; three were newly diagnosed and had not received any treatment. Hypertension was present in nine (26%) but only three (9%) had electrocardiographic left ventricular hypertrophy. Echocardiography showed ventricular hypertrophy in 12 (48%) and increased left ventricular mass in 17 (68%) patients. Holter monitoring detected important ventricular arrhythmias in 14 patients. Thallium-201 scanning showed evidence for coronary heart disease in eight patients. Systolic time intervals were normal except when there was coexistent ischaemic heart disease. A comparison between 19 acromegalic patients with no other detectable cause of heart disease and 22 age matched controls showed appreciably abnormal left ventricular diastolic function in the group with acromegaly. The abnormalities shown did not correlate with left ventricular mass or wall thickness. There was no difference in diastolic function between patients with active acromegaly and those with treated acromegaly. Hypertensive acromegalic patients had worse diastolic function than hypertensive controls, suggesting that hypertension may further impair the left ventricular diastolic abnormality in acromegaly. This is the first study to find evidence of subclinical cardiac diastolic dysfunction in acromegaly and it supports the suggestion that there is a specific disease of heart muscle in acromegaly.     

Influence of obstructive sleep apnea on left ventricular mass and global function: sleep apnea and myocardial performance index

Obstructive sleep apnea (OSA) is associated with cardiovascular mortality and morbidity. It may predispose patients to left ventricular hypertrophy and heart failure. The aim of this study was to determine the left ventricular mass (LVM) and myocardial performance index (MPI) reflecting left ventricular global function in uncomplicated OSA patients. Sixty-four subjects without hypertension, diabetes mellitus, and any cardiac or pulmonary disease referred for evaluation of OSA underwent overnight polysomnography and complete echocardiographic assessment. According to the apnea hypopnea index (AHI), subjects were divided into three groups: group 1, control subjects with nonapneic snorers (AHI < 5, n = 18); group 2, patients with mild to moderate OSA (AHI: 5–30, n = 25); and group 3, severe OSA (AHI > 30, n = 21). Basic echocardiographic measurements, LVM, and LVM index were measured. Left ventricular MPI was calculated as (isovolumic contraction time+isovolumic relaxation time)/aortic ejection time by Doppler echocardiography. There were no significant differences in age, sex, body mass index, heart rate, and systolic and diastolic blood pressure among the three groups. Left atrium, interventricular septum, left ventricular posterior wall, left ventricular end-diastolic and end-systolic diameters, LVM mass, and LVM index were not significantly different among the three groups. Left ventricular MPI was significantly higher in severe OSA patients (0.64 ± 0.18) than in controls (0.49 ± 0.18; P < 0.05). There was no significant difference between controls (0.49 ± 0.18) and mild to moderate OSA (0.61 ± 0.16; P = 0.08) and between mild to moderate OSA (0.61 ± 0.16) and severe OSA (0.64 ± 0.18; P = 0.84). The present study demonstrates that patients with severe OSA have global left ventricular dysfunction.     

Subclinical cardiac dysfunction in acromegaly: evidence for a specific disease of heart muscle.

Acromegaly is associated with an increased cardiac morbidity and mortality, but it is not clear whether this is the result of increased incidence of hypertension and coronary heart disease or of a specific disease of heart muscle. Thirty four acromegalic patients were studied by non-invasive techniques. Seven of these patients had raised plasma concentrations of growth hormone at the time of study; three were newly diagnosed and had not received any treatment. Hypertension was present in nine (26%) but only three (9%) had electrocardiographic left ventricular hypertrophy. Echocardiography showed ventricular hypertrophy in 12 (48%) and increased left ventricular mass in 17 (68%) patients. Holter monitoring detected important ventricular arrhythmias in 14 patients. Thallium-201 scanning showed evidence for coronary heart disease in eight patients. Systolic time intervals were normal except when there was coexistent ischaemic heart disease. A comparison between 19 acromegalic patients with no other detectable cause of heart disease and 22 age matched controls showed appreciably abnormal left ventricular diastolic function in the group with acromegaly. The abnormalities shown did not correlate with left ventricular mass or wall thickness. There was no difference in diastolic function between patients with active acromegaly and those with treated acromegaly. Hypertensive acromegalic patients had worse diastolic function than hypertensive controls, suggesting that hypertension may further impair the left ventricular diastolic abnormality in acromegaly. This is the first study to find evidence of subclinical cardiac diastolic dysfunction in acromegaly and it supports the suggestion that there is a specific disease of heart muscle in acromegaly.     

The relationship between dysglycaemia and cardiovascular and renal risk in diabetic and non-diabetic participants in the HOPE study: a prospective epidemiological analysis

Aims/hypothesis Emerging data suggest that different indices of glycaemia are risk factors for clinical events. The aim of this analysis was to investigate the relationship between fasting plasma glucose or glycated haemoglobin (GHb) levels and incident cardiovascular (CV) outcomes, death, heart failure and overt nephropathy in diabetic and non-diabetic individuals enrolled in the Heart Outcomes Prevention Evaluation (HOPE) study.Materials and methods The adjusted 4.5-year risk of CV events (myocardial infarction or stroke or CV death), heart failure, death and overt nephropathy was analysed in relation to baseline and updated GHb levels (in 3,529 diabetic HOPE study participants) and baseline fasting plasma glucose levels (in 1,937 non-diabetic and 1,013 diabetic participants).Results In diabetic participants, a 1% absolute rise in the updated GHb predicted future CV events (relative risk [RR]=1.07, 95% CI 1.01–1.13; p=0.014), death (RR=1.12, 95% CI 1.05–1.19; p=0.0004), heart failure (RR=1.20, 95% CI 1.08–1.33; p=0.0008) and overt nephropathy (RR=1.26, 95% CI 1.17–1.36; p<0.0001) after adjusting for age, sex, diabetes duration, blood pressure, WHR, hyperlipidaemia and ramipril. Similarly, a 1 mmol/l rise in fasting plasma glucose was related to an increased risk of CV outcomes (RR=1.09, 95% CI 1.05–1.13; p<0.0001), death (RR=1.06, 95% CI 1.01–1.12; p=0.017), heart failure (RR=1.16, 95% CI 1.06–1.13; p=0.0007) and overt nephropathy (RR=1.34, 95% CI 1.23–1.45; p<0.0001) in the group composed of diabetic and non-diabetic individuals. The significant relationship between fasting plasma glucose and CV outcomes persisted after adjustment for diabetes status (RR=1.06, 95% CI 1.00–1.12; p=0.043).Conclusions/interpretation There is an independent progressive relationship between indices of glycaemia and incident CV events, renal disease and death. Clinical trials of glucose lowering to prevent these outcomes in diabetic and non-diabetic individuals are indicated.Listed by country in References 13 and 15.     

Clinical utility of 12-lead electrocardiogram in evaluating heart disease in patients with muscular dystrophy: Assessment of left ventricular hypertrophy,conduction disease,and cardiomyopathy

Introduction

Heart disease remains a leading cause of mortality in patients with muscular dystrophy (MD), and cardiac assessment by standard imaging modalities is challenging due to the prominence of physical limitations.

Methods

In this prospective cohort study of 169 MD patients and 34 negative control patients, we demonstrate the clinical utility of a 12-lead electrocardiogram (ECG) as an effective modality for the assessment of cardiac status in patients with MD. We assessed the utility of conventional criteria for electrocardiogram-indicated left ventricular hypertrophy (ECG-LVH) as well as ECG morphologies.

Results

Cornell voltage, Cornell voltage-duration, Sokolow–Lyon voltage, and Romhilt-Estes point score criteria demonstrated low sensitivity and minimal positive predictive value for ECG-LVH when compared with cardiac imaging. Patients with LBBB had a high probability of a cardiomyopathy (relative risk [RR], 2.75; 95% confidence interval [CI], 2.14–3.53; p < .001), and patients with QRS fragmentation (fQRS) had a high probability of a cardiomyopathy (RR, 1.76; 95% CI, 1.20–2.59; p = .004), requiring cardiac medication and device intervention. We found that an R/S ratio >1 in V1 and V2 is highly specific (specificity, 0.89; negative predictive value [NPV], 0.89 and specificity, 0.82; NPV, 0.89, respectively) for patients with dystrophinopathies compared with other types of MD.

Conclusion

The identification of LBBB and fQRS was linked to cardiomyopathy in patients with MD, while ECG-LVH was of limited utility. Importantly, these findings can be applied to effectively screen a broad cohort of MD patients for structural heart disease and prompt further evaluation and therapeutic intervention.

     

Depressed low frequency power of heart rate variability as an independent predictor of sudden death in chronic heart failure.

AIMS: Identification of patients with chronic heart failure at risk for sudden death remains difficult. We sought to assess the prognostic value for all-cause and sudden death of time and frequency domain measures of heart rate variability in chronic heart failure. METHODS AND RESULTS: We prospectively enrolled 190 patients with chronic heart failure in sinus rhythm, mean age 61+/-12 years, 109 (57.4%) in NYHA class II and 81 (42.6%) in classes III or IV, mean cardiothoracic ratio 57.6+/-6.4% and mean left ventricular ejection fraction 28.2+/-8.8%, 85 (45%) with ischaemic and 105 (55%) with idiopathic dilated cardiomyopathy. Time and frequency domain measures of heart rate variability were obtained from 24 h Holter ECG recordings, spectral measures were averaged for calculation of daytime (1000h-1900h) and night-time (2300h-0600h) values. During follow-up (22+/-18 months), 55 patients died, 21 of them suddenly and two presented with a syncopal spontaneous sustained ventricular tachycardia. In multivariate analysis, independent predictors for all-cause mortality were: ischaemic heart disease, cardiothoracic ratio > or =60% and standard deviation of all normal RR intervals <67 ms (RR = 2.5, 95% CI 1.5-4.2). Independent predictors of sudden death were: ischaemic heart disease and daytime low frequency power <3.3 ln (ms(2)) (RR = 2.8, 95% CI 1.2-8.6). CONCLUSION: Depressed heart rate variability has independent prognostic value in patients with chronic heart failure; spectral analysis identifies an increased risk for sudden death in these patients.     

Transthoracic echocardiographic abnormalities in asymptomatic diabetic patients: association with microalbuminuria and silent coronary artery disease

Aims

This study aimed to assess, on routine echocardiography, cardiac left ventricular (LV) disorders, their determinants and their role in the screening process of silent myocardial ischaemia (SMI) in asymptomatic diabetic patients.

Methods

A total of 586 asymptomatic diabetic patients with one or more additional cardiovascular risk factors, but no history of heart failure or myocardial infarction, prospectively underwent rest echocardiography and myocardial scintigraphy. Those with SMI (abnormal scintigraphy) were subsequently screened for angiographic coronary artery disease (CAD).

Results

LV hypertrophy, LV dilatation, systolic dysfunction and hypokinesia were found in 33.6, 8.6, 3.2 and 6.1%, respectively, of the study population. SMI was found in 156 (26.6%) patients, 55 of whom had silent CAD. On multivariate analysis, age (OR: 1.03 [1.00–1.05], P = 0.02), microalbuminuria (OR: 2.2 [1.4–3.2], P < 0.0001) and silent CAD (OR: 2.4 [1.3–4.6], P = 0.007) were predictive of LV hypertrophy. Creatinine clearance (OR: 0.97 [0.96–0.99], P = 0.002) and silent CAD (OR: 3.7 [1.3–10.0]) were associated with LV dilatation. LV systolic dysfunction was associated with microalbuminuria (OR: 3.8 [1.3–11.4], P = 0.02) and silent CAD (OR: 3.8 [1.1–12.6], P = 0.03). Hypokinesia was associated with retinopathy (OR: 2.4 [1.1–5.4], P = 0.04), microalbuminuria (OR: 2.3 [1.1–5.0], P = 0.04) and LV dilatation (OR: 3.0 [1.1–8.1], P = 0.03). In patients with SMI, the positive predictive value of LV hypertrophy associated with another echocardiographic abnormality (n = 19) for CAD was 63.2%.

Conclusion

LV hypertrophy was found in one-third of asymptomatic diabetic patients, while LV dilatation, systolic dysfunction or hypokinesia was seen in < 10%. The main predictors of LV abnormalities were microalbuminuria and silent CAD. The presence of LV hypertrophy with another abnormality should raise the possibility of the presence of silent CAD.     

Hypertensive heart disease

Hypertensive heart disease encompasses anatomical changes and altered physiology of heart muscle, coronary arteries, and great vessels. Left ventricular hypertrophy is not only a target organ response to increased afterload, but is also the most potent cardiovascular risk factor. Regression of hypertrophy reduces morbidity and mortality. Heart failure may be present in the absence of a reduction of myocardial contractility. Ischemic heart disease occurs in the absence of epicardial coronary disease. Left atrial size and atrial fibrillation are associated. Potentially lethal ventricular arrhythmias and sudden cardiac death are more common in hypertensive patients. The relationship of aortic root size to blood pressure is weaker than expected; however, the relationship to aortic dissection is stronger. Careful attention and treatment of left ventricular hypertrophy, heart failure, ischemic heart disease, and atrial fibrillation will improve survival.     

Outcome of cardiac surgery for carcinoid heart disease

Objectives.The hypothesis was that cardiac surgery for symptomatic carcinoid heart disease in conjunction with adjunctive therapy could improve the long-term outlook of patients with carcinoid heart disease.Background.Patients with carcinoid heart disease have a dismal prognosis; most die of progressive right heart failure within 1 year after onset of symptoms. Improved therapies for the systemic manifestations of the carcinoid syndrome have resulted in symptomatic improvement and prolonged survival in patients without heart disease.Methods.Twenty-six patients with symptomatic carcinoid heart disease underwent valvular surgery. Preoperative clinical, laboratory, Doppler echocardiographic and hemodynamic factors were evaluated. The survival of the surgical group was compared with that of a control group of 40 medically treated patients.Results.There were nine perioperative deaths (35%), primarily from postoperative bleeding and right ventricular failure. Of the 17 surgical survivors, 8 were alive at a mean of 28 months of follow-up. The postoperative functional class of the eight surviving patients was substantially improved. Late deaths were primarily due to hepatic dysfunction caused by metastatic disease. The only predictor of operative mortality (p = 0.03) was low voltage on preoperative electrocardiography (limb lead voltage ≤ 5 mm). Predictors of late survival included a lower preoperative somatostatin requirement and a lower preoperative urinary 5-hydroxy-indoleacetic acid level. There was a trend toward increased survival for the surgical group compared with the control group.Conclusions.Because new therapies have improved survival in patients with the malignant carcinoid syndrome, cardiac involvement has become a major cause of morbidity and mortality. Valve surgery is the only definitive treatment. Although cardiac surgery carries a high perioperative mortality, marked symptomatic improvement occurs in survivors. Surgical intervention should therefore be considered when cardiac symptoms become severe.     

N‐terminal pro‐B‐type natriuretic peptide: an independent marker for coronary artery disease in asymptomatic diabetic patients

Aims To determine whether plasma N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) levels, a marker for cardiac failure and potentially for the severity of coronary artery disease (CAD), predicts silent myocardial ischaemia (SMI) and silent CAD in asymptomatic high‐risk diabetic patients. Methods Five hundred and seventeen asymptomatic diabetic patients with ≥ 1 additional cardiovascular risk factor but without heart failure were prospectively screened between 1998 and 2008 for SMI, defined as an abnormal stress myocardial scintigraphy, and subsequently for significant (> 70%) angiographic CAD. The 323 patients with interpretable echocardiography and for whom NT‐proBNP was measured were included in this analysis. Results SMI was found in 108 (33.4%) patients, 39 of whom had CAD. NT‐proBNP was higher in the patients with CAD than in the patients without CAD [45.0 (1–3199) vs. 20.0 (1–1640) pg/ml; P < 0.0001 median (range)], even after adjustment for confounding factors: age, gender, body mass index, glycated haemoglobin (HbA_1c), retinopathy, nephropathy, hypertension, echocardiographic parameters (P < 0.05). NT‐proBNP in the third tertile (≥ 38 pg/ml) predicted CAD with a sensitivity of 59% and a specificity of 67%. In a multiple logistic regression analysis including NT‐proBNP ≥ 38 pg/ml, age, body mass index, gender, HbA_1c, hypertension, retinopathy, nephropathy, peripheral occlusive arterial disease, left ventricular systolic dysfunction, dilatation and hypertrophy and Type 1 transmitral flow, NT‐proBNP ≥ 38 pg/ml was the only significant independent predictor of silent CAD [odds ratio (OR) 3.1 (95% confidence interval 1.3–7.6), P = 0.015]. Conclusions NT‐proBNP measurement helps to better define asymptomatic diabetic patients with an increased likelihood for CAD, independently of cardiac function and structure.