Search

Increased sympathetic activity may be an underlying mechanism in cardiovascular disease. It has been hypothesized that the degree of left ventricular (LV) hypertrophy is partly related to the blood pressure level, and partly to neurohormonal factors. The aim of this study was to investigate predictors of LV mass, including arterial plasma noradrenaline as an index of sympathetic activity, with particular emphasis on subjects who developed hypertension over a period of 20 years.In a 20-year prospective study of middle-aged men, sustained hypertensives (n = 22), new hypertensives (crossovers) (n = 17) and sustained normotensives (controls) (n = 17) were examined both at baseline and after 20 years of follow-up (at ages 42.1 +/- 0.5 and 62.3 +/- 0.6 years, respectively). Relationships between arterial plasma catecholamines, blood pressure and body mass index at baseline to left ventricular parameters by echocardiography at follow-up were investigated.Groups were homogeneous regarding age, gender, race and body build. The group of sustained hypertensives had significantly more LV hypertrophy (P = 0.025) and diastolic dysfunction (P = 0.010). Among the crossovers, LV mass index was positively correlated to arterial plasma noradrenaline (r = 0.50, P = 0.043) and body mass index (BMI) (r = 0.51, P = 0.039) and showed a positive trend with systolic blood pressure (SBP) at baseline. Arterial plasma noradrenaline (beta = 0.47) was found to predict LV mass index after 20 years independently of BMI (beta = 0.45) and SBP (beta = 0.22) at baseline (R adjusted = 0.345, P = 0.037). Such a relationship was not found in the controls or in the sustained hypertensives, of which 16 were treated with antihypertensive drugs.Arterial plasma noradrenaline at baseline, as an index of sympathetic activity, predicts LV mass at follow-up independently of systolic blood pressure and body build in middle-aged men who developed hypertension over a period of 20 years.

Aortic valve (AV) sclerosis and urine albumin/creatinine ratio (UACR) are both markers of atherosclerosis. We aimed to investigate whether they predicted cardiovascular (CV) events independently in patients with hypertension and electrocardiographic left ventricular (LV) hypertrophy.After 2 weeks of placebo treatment, clinical, laboratory, and echocardiographic variables were assessed in 960 hypertensive patients from the LIFE Echo substudy who had electrocardiographic LV hypertrophy. Morning urine albumin and creatinine were measured calculating UACR. The presence of AV sclerosis was defined as valve thickening or calcification. Fifteen patients with mild AV stenosis were excluded. The patients were followed for 60 +/- 4 months and the composite endpoint (CEP) of CV death, nonfatal stroke, or nonfatal myocardial infarction was recorded.A value of UACR above the median value of 1.406 was associated with higher incidence of CEP and CV death in patients with AV sclerosis (CEP: 18.8% v 9.0% P0.05, CV death: 7.1% v 0.7% P0.01) and in patients without AV sclerosis (CEP: 14.0% v 4.9% P0.001, CV death: 5.1% v 1.1% P0.01). In Cox regression analysis, AV sclerosis predicted CEP (hazard ratio [HR] = 1.52, P.05), but not CV death (HR = 1.30 [0.62 to 2.70], NS) independently of logUACR (HR = 1.70 and HR = 3.25, both P.001). After adjusting for the Framingham Risk Score, CV disease, diabetes, smoking, and treatment allocation, AV sclerosis predicted CEP (HR = 1.5, P.05) but not CV death (HR = 1.4, NS) independently of logUACR (HR = 1.2, P = .09 and HR = 1.94, P.05).In hypertensive patients with electrocardiographic LV hypertrophy, AV sclerosis predicted CEP but not CV death independently of UACR after adjusting for CV risk factors and treatment allocation, indicating that AV sclerosis and UACR might be markers of different aspects of the atherosclerotic process.

This study investigated whether aortic valve (AV) sclerosis was associated with traditional cardiovascular (CV) risk factors and CV events in hypertensive patients with electrocardiographic left ventricular (LV) hypertrophy, as previously demonstrated in the general population. AV sclerosis was associated with several CV risk factors and predicted CV events independently of prevalent CV disease and traditional CV risk factors, including LV mass and ejection fraction.

To assess the prevalence of echocardiographic left ventricular hypertrophy (LVH) and concentric remodeling in hypertensive patients with electrocardiographic (ECG)-LVH and to estimate the cost-effectiveness of echocardiography and ECG for detection of LVH.Echocardiographic LV measurements and the prevalence of abnormal LV geometric patterns were compared between 964 hypertensive patients with ECG-LVH (Cornell voltage-duration product2440 and/or SV1 +/- RV5-638 mm) participating in the LIFE trial and groups of 282 employed hypertensives and 366 apparently normal adults.Among both women and men, stepwise increases from reference subjects to employed hypertensives to LIFE patients were observed for LV wall thicknesses, chamber size and mass. Mean LV mass/body surface area (BSA) and LV mass/height(2.7) were substantially larger in LIFE patients than normal adults among women (113 vs 69 g/m2 and 55 vs 32 g/m(2.7), p0.001) and men (127 vs 83 g/m2 and 55 vs 36 g/m(2.7), p0.001), with intermediate values in employed hypertensives. Compared to the latter group, LIFE patients had higher prevalences of concentric LVH (25-29% vs 3-4%) and eccentric LVH (45-51% vs 13-17%) but not concentric LV remodeling (8-11% vs 12-14%). LVH was present in 70% of LIFE patients by LV mass/BSA criteria and 76% by LV mass/height(2.7) criteria (odds ratios = 11.4 and 13.5 vs employed hypertensives).The ECG criteria used in LIFE identify hypertensive patients with a70% prevalence of anatomic LVH, allowing accurate identification of high-risk status by this commonly used technique.

Decreased plasma concentrations of atrial natriuretic factor (ANF) and of its N-terminal prohormones have been demonstrated in severely hypothyroid patients compared with control subjects, and shown to normalize with thyroxine (T4) replacement therapy. Whether this depends on thyroid hormone deficiency exclusively or is secondary to hemodynamic changes that result from it remains a matter of debate. In a recent investigation dose-related increases in both ANF and N-terminal prohormones of ANF by T4 replacement therapy in incremental doses increased at 4-week intervals were demonstrated. It was suggested that thyroid hormones may enhance synthesis rather than release of atrial peptide hormones. The aim of the present study was to confirm this assumption in hypothyroid patients with normal cardiac performance. Serum N-terminal amino acids 1-98 (ie, pro-ANF 1-98) of pro-ANF was determined in 11 severely hypothyroid patients without pericardial effusion and with normal cardiac left ventricular function. Mean pro-ANF 1-98 concentration before T4 replacement therapy remained unchanged after 10 days on T4 (p = .12). After 2 months of therapy, mean pro-ANF 1-98 was significantly increased compared with pretreatment values (p.003). A significant correlation to the increase in free T4 (r = 0.48, p.01) but not to the decrease in thyrotropin (TSH) (r = -0.32, p = .09) was found. The present results indicate that thyroid hormones directly increase pro-ANF 1-98 independently of cardiac hemodynamics in the hypothyroid state.

Background Advances in the understanding of mitral valve pathology have laid to mitral valve plasty (MPL) as the procedure of choice of all the mitral intervention as compared to mitral valve replacement (MVR). This study is aimed to compare the outcome mortality and reoperation and to estimate failure of repair between the two procedures during the follow up time. Material and methods A cohort of 355 patients with mitral valve disease operated between January 1993 to January 2007 with closing date first of mars 2011. There were 214 MPL and 141 MVR at the Hospital discharge. This retrospective cohort had the design of exposed (MPL) versus non-exposed (MVR) with outcome total mortality and reoperation during follow up. Also echocardiography follow-up was undertaken to estimate the true long-term failure rate of repair. Results The mean follow up was 5.3 years SE (3.82) maximum follow up was 14.1 years. Considering the patient time model the association between repair/replacement and total mortality RR = 0.43 95% (0.28-074) p = 0.002 controlling for the confounding effect of 3-vessels disease. Those results were confirmed by propensity score analysis. As far as outcome re-operation, presence of atrial fibrillation AF was an effect modifier indicating lower reoperation rate for MPL compared to MVR for patients without AF, RR = 0.32 95% CL (0.13-0.81) p = 0.017 while no difference in reoperation rates between MPL/MVR for patients with AF RR = 1.82 95% CL (0.52-6.4) p = 0.344. Echocardiography follows up showed incidence of moderate and severe recurrent mitral regurgitation was 1.34 per 100 patients years and 0.27 per 100 patients years during the follow-up time. Conclusion In a cohort of patient with mitral valve disease undergoing MPL/MVR was examined. MPL was associated with better survival, and lower reoperation rate for patients without AF but same rate for patients with AF. We advocate more attention in controlling risk factors of AF in the clinical management of mitral disease. Long-term failure rate of MPL was low during follow up time. A replication of our results by a randomized clinical trial is mandatory.

In 13 consecutive severely hypothyroid patients no sign of endocrine cardiomyopathy in the form of asymmetric septal hypertrophy (ASH) could be disclosed by M-mode and two-dimensional (2D) echocardiography on examination prior to thyroxine replacement therapy. In previous investigations ASH was demonstrated to be almost invariably present in untreated hypothyroidism irrespective of thyrotropin levels. Consequently application of positive inotropic and afterload reducing agents that may invoke deleterious effects in ASH has been considered hazardous in hypothyroidism even when indicated by concurrent other heart disease. Determination of exact confidence limits reveals that the proportional incidence of hypothyroid hypertrophic cardiomyopathy could not exceed 24.7% with 95% probability. We conclude that ASH is not necessarily inherent in hypothyroidism.

A previously healthy woman in her forties with a six-month history of persistent coughing, breathlessness and fatigue was referred to our hospital for further evaluation. She was initially treated with antibiotics for a possible respiratory tract infection but with only minor effect. A chest x-ray and computer tomography (CT) of the thorax demonstrated a solid tumour in the right lung hilus. Bronchoscopy revealed slight oedema of the bronchial mucous membrane in the area in question. Cytological examination of bronchoalveolar lavage fluid (BAL) showed normal respiratory epithelial cells. Histological examination of a needle biopsy from the tumour showed lymphoproliferative changes of uncertain cause. Magnetic resonance imaging (MRI) of the thorax provided no further information. An electrocardiogram (ECG) revealed signs of left ventricular hypertrophy and sinus bradycardia. Her complaints were palpitations, mild exertional dyspnoea and attenuated heart rate response to exercise. Echocardiography showed increased wall thickness with heterogeneous echogenicity in both ventricles, a slightly enlarged left atrium and mild mitral regurgitation. Tissue Doppler measurements showed impaired relaxation. These findings were suggestive of restrictive cardiomyopathy with diastolic dysfunction. Cardiac MRI confirmed the echocardiographic findings. The tumour was removed by thoracotomy and was shown to be made up of lymphatic tissue with granulomas, consistent with sarcoidosis. The restrictive cardiomyopathy was regarded as a cardiac manifestation of sarcoidosis. The patient was treated with corticosteroids. Clinical follow up with cardiac MRI and echocardiography did not reveal any progression of the cardiac involvement. Cardiac sarcoidosis must be considered in all sarcoid patients because of its significance for prognosis and treatment.

Aims We aimed to compare two-dimensional global longitudinal strain (GS) with different non-invasive imaging modalities for the assessment of left ventricular function in an ST-elevation myocardial infarction population. Methods and results GS was compared with ejection fraction (EF) determined by magnetic resonance imaging (MRI), standard echocardiography (echo), contrast echo, and electrocardiography-gated single-photon emission computed tomography (SPECT), as well as with MRI-determined relative infarct size and echo-determined wall motion score index (WMSI), in 163 patients participating in the NORwegian Study on District Treatment of ST-Elevation Myocardial Infarction (NORDISTEMI). The linear relation between GS and standard echo ( r 2= 0.43, P < 0.001), contrast echo ( r 2= 0.38, P < 0.001), and SPECT-determined EF ( r 2= 0.52, P < 0.001) was almost identical as that between GS and the gold standard MRI-determined EF ( r 2= 0.47, P < 0.001). GS was best associated with WMSI by echo ( r 2= 0.55, P < 0.001), while the associations between GS and relative infarct size were weaker ( r = 0.43, P < 0.001). Receiver operator characteristics curves, used to analyse the ability of GS to discriminate low EF (≤40%) measured by the four different modalities, large myocardial infarction (MI ≥ 15.7%), and high WMSI (≥1.5), were significant for all. GS was shown to be the best predictor of low EF measured by MRI [area under the curve (AUC) 0.965], while the lowest AUC was found between GS and large MI (0.814). Conclusion Global strain is associated well with EF measured by all modalities. Global strain was found to be the best predictor of low EF measured by the gold standard MRI. Since global strain is an inexpensive test, these data may be of health economic interest.

Objectives: The long-term outcome and clinical significance of athlete’s heart has been debated and more longitudinal data are needed. We present a prospective 15 years’ follow-up study of ECG and echo findings in elite endurance athletes following the end of their competitive career. Methods: Clinical evaluation, ECG, ambulatory Holter recording and echocardiography were performed in 30 top-level endurance athletes with a mean age of 24 years with follow-up 15 years later. All had then ended their competitive career, but still performed recreational sports activities. Results: No clinical events were reported. Average resting heart rate was unchanged (53.5 ± 10 at baseline and 55.4 ± 11 at follow-up, p = n.s.), complex ventricular arrhythmias did not occur and the number of ventricular premature beats (VPBs) were 0.4 ± 0.8/h at baseline and 3.8 ± 10/h at follow-up (p = n.s.). In a subgroup of 4 subjects with >100 VPBs per hour at follow-up left ventricular mass was increased compared to the others (p < 0.03). Furthermore, regression of sino-atrial (SA) and atrioventricular (AV) blocks was shown. There were no cases of atrial flutter or fibrillation. There was a slight reduction in mean left ventricular wall thickness (9.9 ± 1.2 vs. 9.5 ± 1.4 mm, p < 0.05) and a highly significant reduction of relative wall thickness (0.38 vs. 0.35, p < 0.001). Left ventricular end-diastolic volume (68 ± 6 vs. 70 ± 7 ml ml/m2, p = n.s.) and left ventricular mass (109 ± 19 vs. 107 ± 19 g/m2, p = n.s.) were unchanged when corrected for body surface area and ejection fraction (EF) increased (60 ± 7 vs. 67 ± 6%, p < 0.01). Parameters of left ventricular diastolic function were normal both at baseline and follow-up. Conclusions: There was no evidence of deleterious cardiac effects of previous top-level endurance athletic activity at 15 years’ follow-up.

Hypertension is one of several risk factors of cardiovascular disease and is associated with left ventricular (LV) systolic and diastolic dysfunction. A method for reliably detecting the onset of LV dysfunction before transition to irreversible damage of the myocardium would be of crucial importance in subjects with essential hypertension.Subjects with clear differences in BP level, development and duration of the hypertensive disease were examined at the age of 60 yrs: normotensives (n = 17), new hypertensives who developed hypertension over a 20 year period (n = 15) and hypertensives (n = 19). Relationships between conventional echocardiographic and tissue velocities imaging (TVI) parameters compared to LV parameters, and TVI as an estimate of LV function were explored. E'(Lat) (TVI peak early diastolic velocity) (P = 0.006) and E/E'(Lat) (P = 0.002) demonstrated differences in diastolic function between the groups. There were no significant differences regarding systolic myocardial velocities. E'(Lat) correlated to S'(Lat) (TDI peak systolic velocity) (r = 0.32, P = 0.026) and was independently predicted by S'(Lat) (R(2) = 0.24, P = 0.025) in multivariate analysis. E'(Lat) correlated negatively to LV mass index (r = -0.34, P = 0.012), also in multivariate regression analysis (R(2) = 0.12, P = 0.032).Myocardial diastolic velocities and mitral flow to annulus velocity ratio differentiated LV function between the hypertensive and normotensive groups. The parameters probably reflect changes in relaxation, recoil and contraction and parallel changes in LV mass index.

To assess the influence of age on changes in left ventricular (LV) mass and geometry during antihypertensive treatment, we related age to clinical and echocardiographic findings before and after 4 years of antihypertensive treatment in a subset of 560 hypertensive patients without known concurrent disease in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, which randomized patients to blinded losartan- or atenolol-based treatment. Patients ⩾65 years (older group) included more women and patients with isolated systolic hypertension or albuminuria (all P

Patients with hypertension have different types of left ventricular (LV) geometry, but the impact of blood pressure (BP) reduction on LV geometry change during antihypertensive treatment remains unclear.Two-dimensional and M-mode echocardiograms were recorded at baseline in 853 unmedicated patients with stage II to III hypertension and LV hypertrophy determined by electrocardiography (Cornell voltage durationor =2440 mV x ms or modified Sokolow-Lyon criteria: SV1 + RV5/RV638 mV) after 14 days of placebo treatment. Follow-up echocardiography was done after 1 year of blinded treatment with either losartan or atenolol, in some cases supplemented with thiazide and calcium antagonist to reach target a BP of 140/90 mm Hg.Baseline systolic/diastolic BP were reduced from 174 +/- 20/95 +/- 11 to 151 +/- 19/84 +/- 11 mm Hg. LV mass was reduced from 234 +/- 56 to 207 +/- 51 g and relative wall thickness from 0.41 +/- 0.07 to 0.38 +/- 0.06 (all P.001). Prevalence of concentric LV hypertrophy decreased from 24% to 6%, eccentric LV hypertrophy from 46% to 37%, and concentric LV remodeling from 10% to 6%; normal geometry increased from 20% to 51%. A shift toward lower LV mass and relative wall thickness was found, as approximately 73% of those with concentric LV remodeling at baseline shifted to normal geometric pattern, whereas only 7% of those with normal pattern at baseline shifted to concentric LV remodeling. Of patients with concentric LV hypertrophy at baseline, 34% shifted to eccentric LV hypertrophy, whereas only 3% with eccentric LV hypertrophy at baseline had concentric LV hypertrophy. Furthermore, multiple regression analysis showed that Doppler stroke volume reduction was a significant correlate of LV mass reduction (beta = 0.108, P.001) independent of BP, heart rate change, and assigned drug treatment.Antihypertensive treatment reduces LV mass and decreases the prevalence of LV hypertrophy and concentric LV remodeling. Additional control of Doppler stroke volume potentiates the effect of BP reduction on LV mass regression independent of the BP reduction per se.

Background — We have shown that hypertensive patients with left ventricular (LV) hypertrophy have decreased LV midwall mechanics, but the effect of antihypertensive therapy remains unclear. Methods and Results — Echocardiograms were recorded at baseline in 679 hypertensive patients and ECG LV hypertrophy and repeated yearly during 3 years of blinded treatment to achieve target blood pressures (BPs) of 140/90 mm Hg. On average, BP was reduced from 174±21 to 147±19 over 95±11 to 82±10 mm Hg and LV mass from 234±56 to 194±50 g. Endocardial fractional shortening (FS) decreased slightly, whereas midwall FS increased from 15.4±2.0% to 16.8±2.1% and stress-corrected midwall FS increased from 97±13 to 105±12% (all P P P P P P Conclusions — Antihypertensive therapy reduced LVM and increased LV midwall shortening and contractility with a small decrease in LV chamber function and significant increase in SV. Change in systolic LV performance was independently associated inversely with change in LVM, RWT, and BP and directly with change in SV.

In some patients with severe hypothyroidism thyroxine replacement therapy precipitates or aggravates angina pectoris, whereas in other patients angina pectoris is ameliorated or even disappears. The reason for this paradox is unknown. It has been attributed either to reversible endocrine cardiomyopathy in the form of asymmetric septal hypertrophy (ASH) or reversible anatomical narrowing of the coronary arteries. The results of a recent investigation, in which myocardial performance was surveyed by radionuclide ventriculography throughout early thyroxine replacement therapy in severe hypothyroidism, were compatible with the presence of reversible coronary dysfunction rather than of ASH. The aim of the present investigation was to confirm these findings. In six severely hypothyroid patients, without echocardiographic evidence of ASH or evidence of concomitant coronary artery disease (CAD), exercise and redistribution tomographic myocardial thallium-201 imaging (SPECT) was performed before thyroxine replacement therapy and repeated after 10 days and again after 2 months during therapy. In four patients substantial regional perfusion defects were demonstrated after exercise that were normalized at rest both before, and in one subject also after 10 days, on thyroxine. With restoration of euthyroidism, exercise and redistribution SPECT were normal in every patient. Determination of exact confidence limits reveals that the proportional incidence of myocardial perfusion defects in hypothyroidism, indicating myocardial ischemia, will at least be 22% with 95% probability. Despite the relatively low specificity of SPECT it seems pertinent to conclude that impaired myocardial perfusion as assessed by SPECT probably is due to reversible coronary dysfunction inherent in the hypothyroid state, and that this is not an infrequent manifestation of severe hypothyroidism.

Thirty top level athletes, 30 athletic students and 30 sedentary controls underwent electrocardiographic and echocardiographic investigation. Resting ECG in athletes showed increased indices of hypertrophy compared to controls. The echocardiographic examination demonstrated an increase in left ventricular mass (LVM) of 47% in top athletes and 23% in athletic students compared to controls. The relationship between wall thickness and diameter was similar in all groups, as were parameters of systolic and diastolic left ventricular function at rest. There was no correlation between LVM assessed by echocardiography and ventricular ectopic activity assessed by Holter monitoring in this normotensive population. Highly significant correlations between ECG and echocardiographic parameters of hypertrophy were demonstrated.

ObjectivesThe aim of this study was to investigate whether myocardial strain echocardiography can predict ventricular arrhythmias in patients after myocardial infarction (MI).BackgroundLeft ventricular (LV) ejection fraction (EF) is insufficient for selecting patients for implantable cardioverter-defibrillator (ICD) therapy after MI. Electrical dispersion in infarcted myocardium facilitates malignant arrhythmia. Myocardial strain by echocardiography can quantify detailed regional and global myocardial function and timing. We hypothesized that electrical abnormalities in patients after MI will lead to LV mechanical dispersion, which can be measured as regional heterogeneity of contraction by myocardial strain.MethodsWe prospectively included 85 post-MI patients, 44 meeting primary and 41 meeting secondary ICD prevention criteria. After 2.3 years (range 0.6 to 5.5 years) of follow-up, 47 patients had no and 38 patients had 1 or more recorded arrhythmias requiring appropriate ICD therapy. Longitudinal strain was measured by speckle tracking echocardiography. The SD of time to maximum myocardial shortening in a 16-segment LV model was calculated as a parameter of mechanical dispersion. Global strain was calculated as average strain in a 16-segment LV model.ResultsThe EF did not differ between ICD patients with and without arrhythmias occurring during follow-up (34 ± 11% vs. 35 ± 9%, p = 0.70). Mechanical dispersion was greater in ICD patients with recorded ventricular arrhythmias compared with those without (85 ± 29 ms vs. 56 ± 13 ms, p < 0.001). By Cox regression, mechanical dispersion was a strong and independent predictor of arrhythmias requiring ICD therapy (hazard ratio: 1.25 per 10-ms increase, 95% confidence interval: 1.1 to 1.4, p < 0.001). In patients with an EF >35%, global strain showed better LV function in those without recorded arrhythmias (−14.0% ± 4.0% vs. −12.0 ± 3.0%, p = 0.05), whereas the EF did not differ (44 ± 8% vs. 41 ± 5%, p = 0.23).ConclusionsMechanical dispersion was more pronounced in post-MI patients with recurrent arrhythmias. Global strain was a marker of arrhythmias in post-MI patients with relatively preserved ventricular function. These novel parameters assessed by myocardial strain may add important information about susceptibility for ventricular arrhythmias after MI.