This study sought to hypothesize that global longitudinal strain (GLS) as a measure of infarct size, and mechanical dispersion (MD) as a measure of myocardial deformation heterogeneity, would be of incremental importance for the prediction of sudden cardiac death (SCD) or malignant ventricular arrhythmias (VA) after acute myocardial infarction (MI).
SCD after acute MI is a rare but potentially preventable late complication predominantly caused by malignant VA. Novel echocardiographic parameters such as GLS and MD have previously been shown to identify patients with chronic ischemic heart failure at increased risk for arrhythmic events. Risk prediction during admission for acute MI is important because a majority of SCD events occur in the early period after hospital discharge.
We prospectively included patients with acute MI and performed echocardiography, with measurements of GLS and MD defined as the standard deviation of time to peak negative strain in all myocardial segments. The primary composite endpoint (SCD, admission with VA, or appropriate therapy from a primary prophylactic implantable cardioverter-defibrillator [ICD]) was analyzed with Cox models.
A total of 988 patients (mean age: 62.6 ± 12.1 years; 72% male) were included, of whom 34 (3.4%) experienced the primary composite outcome (median follow-up: 29.7 months). GLS (hazard ratio [HR]: 1.38; 95% confidence interval [CI]: 1.25 to 1.53; p
Left ventricular diastolic dysfunction (DD) is common after myocardial infarction (MI) despite preservation of left ventricular ejection fraction, yet it remains unclear how or whether DD affects cardiac hemodynamics with stress.
Invasive hemodynamic exercise testing was performed in 46 patients with a recent MI and left ventricular ejection fraction >45% and in 10 healthy volunteers. MI patients were enrolled prospectively and divided into those with DD (MI+DD; left atrial volume index >34 mL/m(2) and diastolic E/e' ratio>8; n=35) and those without DD (MI-DD; left atrial volume index 15 (14?4 mm Hg), whereas none of the MI-DD (10?2 mm Hg) or controls (9?2 mm Hg) displayed pulmonary capillary wedge pressure elevation (P=0.03). During exercise, an abnormal rise in pulmonary capillary wedge pressure (>25 mm Hg) was observed in 94% of MI+DD (36?6 mm Hg) compared with 36% of MI-DD (24?6 mm Hg) and none of the controls (16?6 mm Hg; P
We examined the incidence of new-onset atrial fibrillation in patients with left ventricular dysfunction. Patients either had a recent myocardial infarction (with or without clinical heart failure) or symptomatic heart failure (without a recent MI). Patients were with and without treatment with the class III antiarrhythmic drug dofetilide over 36 months.
The Danish Investigations of Arrhythmia and Mortality ON Dofetilide (DIAMOND) studies included 2627 patients without atrial fibrillation at baseline, who were randomised to treatment with either dofetilide or placebo.
The competing risk analyses estimated the cumulative incidences of atrial fibrillation during the 42 months of follow-up to be 9.6% in the placebo-treated heart failure-group, and 2.9% in the placebo-treated myocardial infarction-group. Cox proportional hazard regression found a 42% significant reduction in the incidence of new-onset AF when assigned to dofetilide compared to placebo (hazard ratio 0.58, 95% confidence interval 0.40-0.82) and there was no interaction with study (p = 0.89). In the heart failure-group, the incidence of atrial fibrillation was significantly reduced to 5.6% in the dofetilide-treated patients (hazard ratio 0.57, 95% confidence interval 0.38-0.86). In the myocardial infarction-group the incidence of atrial fibrillation was reduced to 1.7% with the administration of dofetilide. This reduction was however not significant (hazard ratio 0.61, 95% confidence interval 0.30-1.24).
In patients with left ventricular dysfunction the incidence of AF in 42 months was 9.6% in patients with heart failure and 2.9% in patients with a recent MI. Dofetilide significantly reduced the risk of developing atrial fibrillation compared to placebo in the entire study group and in the subgroup of patients with heart failure. The reduction in the subgroup with recent MI was not statistically significant, but the hazard ratio was similar to the hazard ratio for the heart failure patients, and there was no difference between the effect in the two studies (p = 0.89 for interaction).
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Myotonic dystrophy type 1 (DM1) is associated with increased cardiac morbidity and mortality. Therefore, assessment of cardiac involvement and risk stratification for sudden cardiac death is crucial. Nevertheless, optimal screening-procedures are not clearly defined. ECG, echocardiography and Holter-monitoring are useful but insufficient. Cardiovascular magnetic resonance (CMR) can provide additional information of which myocardial fibrosis may be relevant. The purpose of this study was to describe the prevalence of myocardial fibrosis in patients with DM1 assessed by CMR, and the association between myocardial fibrosis and abnormal findings on ECG, Holter-monitoring and echocardiography.
We selected 30 unrelated patients with DM1: 18 patients (10 men, mean age 51 years) with, and 12 patients (7 men, mean age 41 years) without abnormal findings on ECG and Holter-monitoring. Patients were evaluated with medical history, physical examination, ECG, Holter-monitoring, echocardiography and CMR.
Myocardial fibrosis was found in 12/30 (40%, 9 men). The presence of myocardial fibrosis was associated with the following CMR-parameters: increased left ventricular mass (median (range) 55 g/m² (43-83) vs. 46 g/m² (36-64), p = 0.02), increased left atrial volume (median (range) 52 ml/m² (36-87) vs. 46 ml/m² (35-69), p = 0.04) and a trend toward lower LVEF (median (range) 63% (38-71) vs. 66% (60-80), p = 0.06). Overall, we found no association between the presence of myocardial fibrosis and abnormal findings on: ECG (p = 0.71), Holter-monitoring (p = 0.27) or echocardiographic measurements of left ventricular volumes, ejection fraction or global longitudinal strain (p = 0.18).
Patients with DM1 had a high prevalence of myocardial fibrosis which was not predicted by ECG, Holter-monitoring or echocardiography. CMR add additional information to current standard cardiac assessment and may prove to be a clinically valuable tool for risk stratification in DM1.
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The aim of this study was to assess the epidemiological features and prognosis of heart failure with preserved ejection fraction (HFPEF) and to compare these findings with those from patients with reduced ejection fraction. Furthermore the effects of N-terminal pro brain natriuretic peptide (NT-proBNP) requirement in the heart failure diagnosis were assessed by repeating the analyses in the subgroup of patients with elevated NT-proBNP.
In 1844 patients admitted, a clinical diagnosis of heart failure was made in 433; amongst these 61% had HFPEF. An elevated NT-proBNP applied to the heart failure diagnosis reduced the number of heart failure patients to 191, and amongst these 29% had preserved ejection fraction. Use of NT-proBNP reduced clinical differences between heart failure patients with preserved and reduced ejection fraction. When not using NT-proBNP, patients with reduced ejection fraction had higher mortality [hazard ratio (HR) 1.24, 95% confidence interval (CI) 1.01-1.52; P = 0.04], even after adjustment for other significant predictors of mortality, except NT-proBNP (HR 1.29, 95% CI 1.04-1.59; P = 0.02). However, no difference in mortality was observed when NT-proBNP was adjusted for (HR 0.90, 95% CI 0.71-1.15; P = 0.4), or used for the heart failure diagnosis (HR 0.96; 95% CI 0.71-1.29; P = 0.8).
Using a heart failure diagnosis requiring elevated NT-proBNP reduces the prevalence of HFPEF and results in a survival similar to that of heart failure with reduced ejection fraction. In contrast, when NT-proBNP is not used for the heart failure diagnosis or adjusted for, HFPEF is associated with a lower mortality in both univariate and multivariate analysis.
Hypertension is a common comorbidity in patients with heart failure and may contribute to development and course of disease, but the importance of a history of hypertension in patients with prevalent heart failure remains uncertain.
3078 consecutively hospitalized heart failure patients (NYHA classes II-IV) were screened for the EchoCardiography and Heart Outcome Study (ECHOS). The left ventricular ejection fraction (LVEF) was estimated by 2 dimensional transthoracic echocardiography in all patients and a subgroup of 878 patients had additional data on pulsed wave Doppler assessment of transmitral flow available. A restrictive filling (RF) was defined as a mitral inflow deceleration time =140 ms. Patients were followed for a median of 6.8 (Inter Quartile Range 6.6-7.0) years and multivariable Cox regression models were used to assess the risk of all-cause mortality associated with hypertension.
The study population had a mean age of 73 ± 11 years. 39% were female, 27% had a history of hypertension and 48% had a RF. Over the study period, 64% of the population died. Hypertension was not associated with increased risk of mortality, hazard ratio (HR) 0.95 (0.85-1.05). LVEF did not modify this relationship (p for interaction = 0.7), but RF pattern substantially influenced the outcomes associated with hypertension (p for interaction
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To study whether there is interaction between mitral regurgitation (MR) and left ventricular ejection fraction (LVEF) in the mortality risk of heart failure (HF) patients.
We studied a large group of patients hospitalized for symptoms and clinical signs of HF in the period 2001-02. Mitral regurgitation was diagnosed on echocardiography and qualitatively graded as no/trace, mild, moderate, and severe using the colour Doppler method. Median follow-up time was 4.5 years. Three thousand and seventy-eight patients with HF were included, of whom 1890 patients (61%) had no/trace MR, 628 (20%) had mild MR, 452 (15%) had moderate MR, and 108 (4%) had severe MR. During follow-up, 1660 deaths (54%) were registered. In univariate analysis, increasing severity of MR carried an increasing mortality risk, hazard ratio (HR) 1.10, 95% confidence interval (CI) 1.04-1.16, P = 0.0006 for each increasing degree of MR. In multivariable analysis, with adjustments made for age, sex, ejection fraction, serum creatinine, presence of ischaemic heart disease, chronic obstructive pulmonary disease, diabetes, and stroke, similar results were found, but only in patients with LVEF
Renal dysfunction is associated with a variety of cardiac alterations including left ventricular (LV) hypertrophy, LV dilation, and reduction in systolic and diastolic function. It is common and associated with an increased mortality risk in heart failure (HF) patients. This study was designed to evaluate whether severe diastolic dysfunction contribute to the increased mortality risk observed in HF patients with renal dysfunction.
Using Cox Proportional Hazard Models on data (N = 669) from the EchoCardiography and Heart Outcome Study (ECHOS) study we evaluated whether estimated glomerular filtration rate (eGFR) was associated with mortality risk before and after adjustment for severe diastolic dysfunction. Severe diastolic dysfunction was defined by a restrictive left ventricular filling pattern (RF) (=deceleration time
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Targeted temperature management at 33°C versus 36°C and impact on systemic vascular resistance and myocardial function after out-of-hospital cardiac arrest: a sub-study of the Target Temperature Management Trial.
Cardiovascular dysfunction is common after out-of-hospital cardiac arrest as part of the postcardiac arrest syndrome, and hypothermia may pose additional impact on hemodynamics. The aim was to investigate systemic vascular resistance index (SVRI), cardiac index, and myocardial performance at a targeted temperature management of 33°C (TTM33) versus 36°C (TTM36).
Single-center substudy of 171 patients included in the Target Temperature Management Trial (TTM Trial) randomly assigned to TTM33 or TTM36 for 24 hours after out-of-hospital cardiac arrest. Mean arterial pressure =65 mm Hg and central venous pressure of 10 to 15 mm Hg were hemodynamic treatment goals. Hemodynamic evaluation was performed by serial right heart catheterization and transthoracic echocardiography. Primary end point was SVRI after 24 hours of cooling and secondary end points included mean SVRI, cardiac index, systolic function, and lactate levels. The TTM33 group had a significant increase in SVRI compared with TTM36 (2595; 95% confidence interval, 2422-2767) versus 1960 (95% confidence interval, 1787-2134) dynes m(2)/s per cm(5); P