Outcome of mitral valve plasty or replacement: atrial fibrillation an effect modifier.

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). 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. 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.

[A woman with a chronic cough and dyspnoea]. / En kvinne med kronisk hoste og dyspné.

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.

Assessment of left ventricular function in ST-elevation myocardial infarction by global longitudinal strain: a comparison with ejection fraction, infarct size, and wall motion score index measured by non-invasive imaging modalities.

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.

Mechanical dispersion assessed by myocardial strain in patients after myocardial infarction for risk prediction of ventricular arrhythmia.

OBJECTIVES: The aim of this study was to investigate whether myocardial strain echocardiography can predict ventricular arrhythmias in patients after myocardial infarction (MI). BACKGROUND: Left 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. METHODS: We 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. RESULTS: The 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). CONCLUSIONS: Mechanical 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.

Long-term assessment of electrocardiographic and echocardiographic findings in Norwegian elite endurance athletes.

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/m(2), p = n.s.) and left ventricular mass (109 +/- 19 vs. 107 +/- 19 g/m(2), 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.

Arterial plasma noradrenaline predicts left ventricular mass independently of blood pressure and body build in men who develop hypertension over 20 years.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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 sclerosis and albuminuria predict cardiovascular events independently in hypertension: a losartan intervention for endpoint-reduction in hypertension (LIFE) substudy.

BACKGROUND: 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. METHODS: 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. RESULTS: 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% P < 0.05, CV death: 7.1% v 0.7% P < 0.01) and in patients without AV sclerosis (CEP: 14.0% v 4.9% P < 0.001, CV death: 5.1% v 1.1% P < 0.01). 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). CONCLUSIONS: 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.

Aortic valve sclerosis relates to cardiovascular events in patients with hypertension (a LIFE substudy).

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.

Relation of impaired left ventricular filling to systolic midwall mechanics in hypertensive patients with normal left ventricular systolic chamber function: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study.

BACKGROUND: Patients with hypertensive left ventricular (LV) hypertrophy commonly have diastolic dysfunction with preserved LV ejection fraction. LV systolic midwall shortening (MWS) may be impaired in hypertensive patients with normal LV ejection fraction. However, it is unclear whether impaired LV filling is related to depressed systolic midwall mechanics. METHODS: Echocardiographic measures of LV diastolic filling and systolic performance were compared in 632 unmedicated patients with stage II or III hypertension and LV hypertrophy determined by electrocardiogram, with LV ejection fraction >55% and <2+ mitral regurgitation. RESULTS: Stress-corrected LV MWS, an index of myocardial contractility, was lower in patients with abnormal as opposed to normal LV filling patterns (98% +/- 12% vs 102% +/- 10%, P <.001) and in patients with prolonged as opposed to normal isovolumic relaxation time (IVRT) (98% +/- 13% vs 101% +/- 12%, P =.014). Stress-corrected MWS was <85% of predicted levels in more patients with abnormal LV filling patterns (11.8% vs 6.3%) or with long IVRT (> or =105 msec) (34% vs 21%, both P <.05). In regression analyses, lower stress-corrected MWS and higher LV mass were independent correlates of longer IVRT, while lower stress-corrected MWS was the only independent correlate of prolonged mitral valve deceleration time (P =.017). Higher LV mass had strong, statistically independent relationships to longer IVRT (by 0.3 g/msec) and decreased stress-corrected MWS (by 0.5 g/%; both P <.0001), independent of body size and age. CONCLUSION: In patients with moderate hypertension and target organ damage who have normal LV ejection fraction, impaired early diastolic LV relaxation (abnormal E/A ratio, prolonged IVRT and deceleration time) is associated with impaired LV systolic midwall mechanics independent of higher LV mass.

Change of left ventricular geometric pattern after 1 year of antihypertensive treatment: the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study.

BACKGROUND: 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. METHODS: 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 duration > or =2440 mV x ms or modified Sokolow-Lyon criteria: SV1 + RV5/RV6 >38 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. RESULTS: 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. CONCLUSIONS: 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.

Change in systolic left ventricular performance after 3 years of antihypertensive treatment: the Losartan Intervention for Endpoint (LIFE) Study.

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<0.001). Change in midwall FS was related inversely to change in LV mass (LVM), relative wall thickness (RWT), and diastolic BP and directly to change in Doppler stroke volume (SV, all P<0.001). Multivariate analysis showed that change in MWS was independently inversely related to changes in LVM (beta=-0.211), RWT (beta=-0.334, all P<0.001), and diastolic BP (beta=-0.088, P<0.05) and directly related to SV (beta=0.192, P<0.001) with control for blinded therapy. Change in stress-corrected midwall shortening was inversely independently associated with changes in LVM (beta=-0.153) and RWT (beta=-0.562) and directly with changes in SV (beta=0.145) and systolic BP (beta=0.s221, all P<0.001) with control for blinded therapy. 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.