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AimsTo identify carriers and non-carriers of the mutant transthyretin methionine 111 linked familial amyloid disease, to detect early signs of the restrictive cardiomyopathy and other clinical manifestations characteristic of this inheritable diseaseMethods and ResultsOut of 125 living family members 99 were available for clinical, echocardiographic and genetic examination. Twenty-five family members were heterozygous carriers of the mutant transthyretin methionine 111 genotype, while 74 were non-carriers. Among the 25 carriers, none had overt clinical signs of heart disease. Eight carriers, all above the age of 35, showed echo-cardiographic abnormalities suggestive of developing or manifest restrictive cardiomyopathy. Three had biopsy-verified transthyretin-related amyloid cardiomyopathy. None of the 15 carriers in the younger age group exhibited aberrant echocardiographic patterns. Nine carriers had carpal tunnel syndrome as opposed to none of the non-carriers.ConclusionFor early detection of familial amyloid cardiomyopathy, echocardiography is the investigation of choice. The first sign is diastolic dysfunction detected as an abnormal relaxation pattern. The appearance of echo-cardiographic aberrations solely in the older age group suggests that the cardiomyopathy is a late onset disease. Carpal tunnel syndrome appears to be the earliest presenting clinical symptom. A curative treatment seems to be an early liver transplantation. [ABSTRACT FROM PUBLISHER]

Current guidelines recommend angiotensin receptor blocker neprilysin inhibitors (ARNI) (sacubitril/valsartan) as a replacement for angiotensin-converting-enzymeinhibitor (ACE-I) in heart failure with reduced ejection fraction (HFrEF) who remain symptomatic despite optimal medical therapy. The effects of ARNIs have not previously been assessed in a systematic review. We searched for relevant trials until October 2019 in CENTRAL, MEDLINE, Embase, LILACS, BIOSIS, CNKI, VIP, WanFang and CBM. Our primary outcomes were all-cause mortality and serious adverse events. We systematically assessed the risks of random errors and systematic errors. PROSPERO registration: CRD42019129336. 48 trials randomising 19 086 participants were included. The ARNI assessed in all trials was sacubitril/valsartan. ACE-I or ARB were used as control interventions. Trials randomising HFrEF participants (27 trials) and heart failure with preserved ejection fraction (HFpEF) participants (four trials) were analysed separately. In HFrEF participants, meta-analyses and Trial Sequential Analyses showed evidence of a beneficial effect of sacubitril/valsartan when assessing all-cause mortality (risk ratio (RR), 0.86; 95% CI, 0.79 to 0.94) and serious adverse events (RR, 0.89; 95% CI, 0.86 to 0.93); and the results did not differ between the guideline recommended target population and HFrEF participants in general. We found no evidence of an effect of sacubitril/valsartan in HFpEF participants. Sacubitril/valsartan compared with either ACE-I or ARB seems to have a beneficial effect in patients with HFrEF. Our results indicate that sacubitril/valsartan might be beneficial in a wider population of patients with heart failure than the guideline recommended target population. Sacubitril/valsartan does not seem to show evidence of a difference compared with valsartan in patients with HFpEF., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Rationale & Objective: Left ventricular (LV) mass (LVM) is a predictor of cardiovascular morbidity and mortality and commonly calculated using 1-dimensional (1D) echocardiographic methods. These methods are vulnerable to small measurement errors and LVM may wrongly change according to changes in LV volume (LVV). Less commonly used 2-dimensional (2D) methods can accommodate to the changes in LVV and may be a better alternative among patients receiving hemodialysis (HD) with large fluid fluctuations., Study Design: Observational study., Setting & Participants: Patients with end-stage kidney disease receiving HD., Exposure: One HD session., Analytical Approach: Transthoracic echocardiography was performed right before and after HD. LVM was calculated using 1D (Devereux, Penn, and Teichholz) and 2D methods (truncated ellipsoid and area-length)., Outcomes: Significant differences in LVM after HD., Results: We compared dimensions, LVV and LVM, in 53 patients (mean age, 63 ± 15 years; 66% men). For each 1-L increase in ultrafiltration volume (UFV), LV internal diameter decreased 1.1 mm (95% CI, 0.5-1.7 mm; P  = 0.001). Patients were divided into 2 groups by the median UFV of 1.6 L. Patients with UFV > 1.6 L had significant smaller LVV and LV internal diameter after HD. LVM calculated using 1D methods decreased according to changes in LVV. Conversely, LVM calculated using 2D methods was not significantly different after HD. No significant change in differences between diastolic - systolic myocardial thickness or LVM as assessed using 1D and 2D methods was observed before and after HD, indicating that LVM remained constant despite HD., Limitations: We did not use contrast enhancement, 3-dimensional methods, or cardiac magnetic resonance., Conclusions: LVM calculated using 2D methods, truncated ellipsoid and area-length, is less affected by fluctuations in fluid and LVV, in contrast to 1D methods. Complementary LVM calculation using 2D methods is encouraged, especially in patients with large fluid fluctuations in which increased LVM using a 1D method has been detected., (© 2020 The Authors.)

Background: The value of N-terminal pro-brain natriuretic peptide (NT-proBNP) in terms of diagnosis and prognosis in congestive heart failure (CHF) and left ventricular systolic dysfunction (LVSD) has been demonstrated previously in various populations, but data on primary care patients are sparse. The aim of this study was to evaluate the diagnostic and prognostic performance of NT-proBNP in primary care patients with suspected CHF., Methods and Results: Three hundred sixty-seven consecutive patients (mean age, 68.8 years; range, 39.0-84.0 years) who had been referred by their general practitioner for echocardiographic evaluation because of suspected CHF. In all patients, NT-proBNP was measured at baseline and left ventricular ejection fraction (LVEF) was estimated with echocardiography. LVSD (LVEF < or =0.40) was found in 9% of the patients. NT-proBNP was significantly higher in patients with LVSD (P < .0001). With predefined cut off values for NT-proBNP (125 pg/mL), the sensitivity, specificity, positive predictive value, and negative predictive value for the detection of LVSD were 0.97, 0.46, 0.15 and 0.99, respectively. Area under the receiver operating characteristic curve was 0.87. The application of an age-differentiated cut-off value for NT-proBNP (125 pg/mL for <75 years old and 450 pg/mL for > or =75 years old) did not increase diagnostic performance. Patients were followed for a median of 778 days; 8% of the patients died during the follow-up period. The mortality rate was higher in patients with NT-proBNP of >125 pg/mL than in patients with normal values (P < .002, log rank), and the difference persisted after controlling for age, gender, and LVEF (hazard ratio per unit increase in log NT-proBNP, 2.2; range, 1.2-4.1; P = .015)., Conclusion: In primary care patients who were referred for echocardiography because of suspected CHF, NT-proBNP values <125 pg/mL effectively rule out LVSD. Furthermore low NT-proBNP values are associated with a lower risk of death, independently of age, gender, and LVEF.

Objective: To characterise the effect of long-term low-dose growth hormone (GH) treatment on cardiac anatomy and function., Methods: 20 patients with multiple pituitary hormone deficiencies, including severe acquired GH deficiency (GHD), were randomly assigned to GH or placebo (P) for 18 months. Echocardiographic measurements were performed at baseline and after 6, 12 and 18 months., Results: At baseline, 8 of 20 patients had diastolic dysfunction (6 severe and 2 borderline), while only 1 had systolic dysfunction. None of the investigated parameters of diastolic or systolic function changed during treatment., Conclusion: In adult onset GHD, diastolic dysfunction was present in 40% of the patients. None of the investigated values were different after 18 months of GH compared to placebo., (Copyright 2002 S. Karger AG, Basel)

Objective: To compare the effect of a calcium antagonist and a beta-blocker on left-ventricular diastolic function in patients with ischemic heart disease., Methods: 138 patients with chronic stable angina pectoris were randomized in a multicenter, double-blind trial to treatment with either mibefradil or atenolol for 6 weeks (50 mg once daily for 2 weeks followed by 100 mg once daily for 4 weeks). The ratio between early (E) and late (A) diastolic mitral flow velocities (E/A), the E wave deceleration time (DT) and the left ventricular isovolumetric relaxation time (IRT) were measured by Doppler echocardiography as parameters of left-ventricular diastolic function initially, after 4 and after 6 weeks of treatment., Results: Mibefradil did not change the E/A ratio significantly (+4%, NS), while atenolol treatment resulted in a significant increase in the E/A ratio (+20%, p < 0.001). Mibefradil treatment, on the other hand, resulted in a significant decrease (-8%, p < 0.001) in IRT, while atenolol treatment did not change IRT. Neither mibefradil nor atenolol treatment changed DT significantly., Conclusions: Both mibefradil and atenolol treatment significantly improves echocardiographic indices of left-ventricular diastolic function in patients with chronic stable angina. However, they affect different parameters and thus apparently act through different mechanisms., (Copyright 2001 S. Karger AG, Basel)

Purpose: To examine the influence of (i) strong predisposition to essential hypertension and (ii) insulin sensitivity and plasma levels of cardiomyotrophic hormones on echocardiographic parameters of left ventricular structure and function., Methods: 26 normotensive subjects (age 18-35) with bi-parental hypertension and 26 matched controls with normotensive parents. Families with non-insulin-dependent diabetes or morbid obesity were excluded. (i) Echocardiography; (ii) plasma concentrations of renin, angiotensin-II, aldosterone, epinephrine and norepinephrine; (iii) euglycaemic, hyperinsulinemic clamp study. RESULTS (means +/- SD): Hypertension-prone subjects vs controls had (i) higher resting systolic (117.0 +/- 14.0 vs 107.1 +/- 11.9 mmHg), and 24-h diastolic blood pressure (77.9 +/- 7.1 vs 72.9 +/- 7.2 mmHg), (ii) higher relative wall thickness (RWT) (0.39 +/- 0.09 vs 0.34 +/- 0.06). They had similar left vetricular mass index, diastolic function parameters, insulin sensitivity and plasma concentrations of cardiomyotrophic hormones. The increased RWT was not attributable to any other factor than the systolic blood pressure., Conclusion: In a carefully selected group of subjects with two hypertensive parents compared to a control group, the only echocardiographic change demonstrated was an increased RWT. This remodelling was attributable to a higher systolic blood pressure in the hypertension-prone subjects, but not to insulin sensitivity or a selection of cardiomyotrophic hormones.

Amyloidosis is a group of diseases characterized by amyloid deposition in various tissues. The diseases can roughly be divided into hereditary and non-hereditary forms. The hereditary forms are related to a mutation in the serum protein transthyretin which is produced mainly in the liver. The inheritance is autosomal dominant. A family in Denmark has earlier been described as having inherited cardiac amyloidosis with a mutation at amino acid number 111 in the transthyretin protein. The family now has been re-examined because of new diagnostic and therapeutic possibilities. The aims of the study were to identify carriers and non-carriers of the mutant transthyretin methionine 111 linked familial amyloid disease, to detect early signs of the restrictive cardiomyopathy and other clinical manifestations of this disease. Clinical, echocardiographic and genetic examination was carried out. Out of 125 living family members, 99 were available for examination. Twenty-five persons were heterozygous carriers of the mutant transthyretin methionine 111 genotype, while 74 were non-carriers. Eight carriers, all above the age of 35, showed echocardiographic abnormalities suggestive of developing or manifest restrictive cardiomyopathy. Nine carriers had carpal tunnel syndrome as opposed to none of the non-carriers. It is concluded that for early detection of familial amyloid cardiomyopathy, echocardiography is the investigation of choice. The first sign is diastolic dysfunction detected as an abnormal relaxation pattern. Carpal tunnel syndrome appears to be the earliest presenting clinical symptom. Early liver transplantation seems to be curative.

In spring 1997, all medical departments in Denmark and the Faroe Islands, not including cardiological centers, were asked to reply to a questionnaire concerning their ability to perform echocardiography at hours different from normal daytime. The response rate was 94.5%. In 21 (30.4%) of 69 departments none of the senior doctors on duty were able to perform echocardiography. In only eight (11.6%) of the departments were more than 50% of the senior doctors on duty able to perform echocardiography (M-mode/2D). Echocardiography is the most informative investigation for patients with suspected acute heart failure or with acute dyspnoea of unknown cause. In these cases acutely performed echocardiography will often be of critical diagnostic value and thereby deciding for correct and rapid therapy. This investigation shows that only a very small fraction of the medical departments in Denmark are able to perform acute echocardiography on a 24-hour basis.

The aim of the study was to assess the diagnostic value of bicycle exercise echocardiography using quantitative coronary arteriography as a reference. Exercise echocardiography was performed in 70 consecutive patients referred for coronary angiography. Digital loops were obtained at rest, peak, and immediately after exercise in the standard views (parasternal long and short axis, apical two and four chamber views). Wall motion analysis was made on the basis of the 16 segment model, scoring each segment from 3 (hyperkinesia) to -1 (hypokinesia). Exercise echocardiography was considered positive when wall motion in at least one segment decreased at least one score from rest to peak or post exercise. Cinefilms were evaluated using automated quantitative coronary arteriography software. Transstenotic pressure gradients were calculated based on flow assumptions at the maximal stenosis flow reserve. Pressure losses > 30 mmHg and quantitatively measured percent diameter stenosis of > 50% were considered clinically significant. Stenoses in the equivocal range of 40-69% were subjected to separate analysis. Exercise echocardiography was superior to exercise-induced ST-segment depression in the diagnosis of coronary artery disease. In the overall sample of 70 patients, the sensitivity of exercise echocardiography against percent diameter stenosis was 84%, against pressure gradient 86%. The specificity against these two parameters was 86% and 84%, respectively. When analysing the subgroup of 40-69% stenoses (N = 14), sensitivity of exercise echocardiography against percent diameter stenosis was 67%, against pressure gradient 88%. The specificity against these two parameters was 100% and 84%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Dobutamine stress echocardiography (DSE) is a new diagnostic method for evaluation of patients with known or suspected coronary artery disease. We studied 30 consecutive patients referred for evaluation of chest pain. Coronary angiography was carried out in 28 patients. DSE was performed the following day. Readable echocardiographic recordings were obtained in all patients. Blinded wall motion analysis revealed a diagnostic sensitivity of 91% (95% confidence limits: 79-100%) for dobutamine stress echocardiography using coronary angiography as reference. No severe adverse events or arrhythmias occurred. It is concluded that DSE is well tolerated, feasible and has a high sensitivity for detecting coronary artery disease.

The aim of our study was to assess the diagnostic value of exercise echocardiography compared with exercise ECG and coronary arteriography. Exercise echocardiography was performed in 60 consecutive patients referred for coronary arteriography because of suspected coronary artery disease. Echocardiography was carried out in combination with bicycle exercise ECG and was performed 1) at rest before exercise with the patient supine, 2) at peak exercise on the bicycle and 3) immediately after exercise in supine position. Conventional standard views were recorded by means of an image computer. For the regional wall motion analysis, images were displayed simultaneously from the rest, peak and post exercise situations in a quadscreen format. Ischemia was diagnosed when wall motion deteriorated from rest to peak or post exercise in at least one out of a total of 16 left ventricular segments. Analysis was made without knowledge of patient data or results of exercise ECG or coronary arteriography. No patient was excluded because of reduced echocardiographic image quality during exercise or other technical reason. Coronary arteriography was performed in all patients and used as reference. The sensitivity of exercise echocardiography was 91% and the specificity 100%. The predictive value of a positive test was 100% and the predictive value of a negative test 78%. For exercise ECG the corresponding values were 58%, 100%, 100% and 39% respectively. We conclude that exercise echocardiography seems to be useful for the diagnosis and exclusion of ischemic heart disease. This and other studies indicate that the method is more sensitive than exercise ECG.

The purpose of this study was to define the prognostic value concerning in-hospital, two-month, and one-year mortality of an early echocardiographic estimation of left ventricular ejection fraction, relative to traditional clinical variables and a clinical prognostic index, in an unselected series of 193 patients following acute myocardial infarction. Left ventricular ejection fraction was determined within 72 hours by echocardiographic wall motion analysis within the frame of a nine-segment model. Clinical variables (age, number of acute myocardial infarctions, reinfarction, heart failure, cardiac arrest, ventricular arrhythmias, asystole, supraventricular tachycardia, nodal rhythm) and a calculated, previously published index, based on these variables, were recorded on day five post infarction and predischarge. The Killip class was recorded at the time of echocardiography. All variables were compared by a multivariate approach (Cox regression model). The results showed that left ventricular ejection fraction was the strongest predictor of early and late mortality and increasingly so over the period of observation. Age and maximal Killip class had a modest additional prognostic value, whereas the composite clinical prognostic index had no predictive power when early left ventricular ejection fraction was included in the statistical model.

The relative prognostic value of clinical heart failure and early M-mode and 2-dimensional echocardiographic indexes of left ventricular performance was compared in a study of 205 consecutive patients with acute myocardial infarction (AMI). Statistical analysis showed that an early wall motion score was a stronger predictor of 1-year mortality than the occurrence of clinical heart failure early, late or at any time during the hospital course of AMI. The finding of clinical heart failure had an independent prognostic value of intermediate strength. M-mode echocardiographic parameters only had a weak independent prognostic value, possibly related to their content of information on left ventricular end-systolic dimension.

To determine the prognosis of late ventricular fibrillation (VF) after acute myocardial infarction (AMI), the length of the monitoring period after AMI was extended. All patients in this series were continuously monitored in a coronary care unit to ensure observation of all VF within 18 days of AMI. From 1977 to 1985, 4,269 patients were admitted with AMI and 413 (9.6%) had in-hospital VF. Of these 281 (6.8%) had early VF (less than 48 hours after AMI) and 132 (3.2%) had late VF (greater than or equal to 48 hours after AMI). In-hospital mortality was 50 and 54% for early and late VF, respectively (p = 0.31). Kaplan-Meier survival analysis showed better survival after discharge for patients with early versus late VF (p = 0.009) but this difference was fully explained by the presence of heart failure. Survival analysis showed the same prognosis after 1, 3 and 5 years for early and late VF, when VF was not associated with heart failure. When VF was associated with heart failure (secondary VF) early VF had a greater mortality than late VF after 2 and 5 years. Logistic regression analysis showed that heart failure (relative risk 1.9 [1.1 to 3.1]) and cardiogenic shock (relative risk 3.9 [1.8 to 8.5]) were significant risk factors for in-hospital death. Late VF compared to early VF had no prognostic implication (relative risk 1.0 [0.6 to 1.6]). For patients discharged from the hospital, risk factors were heart failure (1.8 [1.1 to 2.8]) and previous AMI (1.6 [1.3 to 2.1]).(ABSTRACT TRUNCATED AT 250 WORDS)

In a prospective series of 201 consecutive patients with creatine kinase-MB--documented acute myocardial infarction (AMI), postadmittance and predischarge echocardiographic wall motion indexes (WMI) were determined (median 45 hours vs 14 days after AMI). No significant change of left ventricular systolic performance was found between postadmittance and predischarge examinations in 179 survivors (WMI 1.3 +/- 0.4 vs 1.4 +/- 0.4, p greater than 0.05). Hospital mortality was 11% (22 of 201), cumulated 2-month mortality 15% (31 of 201) and cumulated 1-year mortality 26% (52 of 201). Mortality increased rapidly with decreasing left ventricular function as determined by WMI. When early WMI was less than 1.0, 1-year mortality was 51% (28 of 55) versus 8% (7 of 83) when WMI was greater than 1.3 (p less than 0.0001). Ventricular fibrillation (n = 24) and cardiogenic shock (n = 27) carried a much better prognosis when WMI showed good left ventricular function. When WMI was less than 1.0, 1-year mortality was 83% (10 of 12) versus 93% (13 of 14) in ventricular fibrillation and cardiogenic shock, respectively, whereas it was 0% (0 of 4) versus 33% (2 of 6) when WMI was greater than 1.3. In 15% of patients major discrepancies between early Killip class and WMI were noted. WMI showed much smaller fluctuations during the hospital course of AMI than did Killip class and appeared to be a more stable prognostic marker. Large-scale, early risk stratification by echocardiography has now become available and appears to facilitate a rational, individualized discharge policy in the coronary care unit and to provide an improved basis for randomization of patients in controlled studies aimed at tailoring new treatment in AMI.

The value of radiographic examination of the thorax, fluoroscopy and echocardiography in demonstration and localization of intracardiac calcifications were compared in an investigation of 40 patients with valvular heart disease prior to planned cardiac catheterization or operation. Radiographic examination of the thorax revealed only the most severe calcifications. By means of echocardiography it proved possible to undertake a simple semi-quantitative characterisation of the calcified tissue with acceptable intra- and inter-observer variation. Echocardiography and fluoroscopy were found to be of equal value in demonstration of the degree of calcification of the heart. Echocardiography was, however, superior to fluoroscopy in fine localization of the calcifications. The relative and additive values of the methods could be illustrated employing Bayes' theorem and could be represented graphically provided that the observations carried out with the three methods could be considered independent of one another. It is concluded that radiographic examinations of the thorax is unsuitable for screening for cardiac calcifications. Fluoroscopy can no longer be considered to be the method of choice in assessing lesions of this type but should be employed in cases where echocardiography does not provide sufficient information or is not available. The greatest certainty in demonstration of calcifications is obtained with combined employment of fluoroscopy and echocardiography.