| 1. |
- Guron, Cecilia Wallentin, 1965, et al.
(författare)
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Usefulness of atrial size inequality as an indicator of abnormal left ventricular filling
- 2005
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Ingår i: Am J Cardiol. - : Elsevier BV. - 0002-9149. ; 95:12, s. 1448-52
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Tidskriftsartikel (refereegranskat)abstract
- Although pulsed Doppler echocardiography estimates current left ventricular (LV) filling, left atrial (LA) size reflects LV filling and pressure over time. However, the wide normal LA size range may blunt this diagnostic tool. Our objective was to compare the intraindividual atrial area difference (LA--right atrial [RA] area) and absolute LA area in their detection of a LA enlargement with respect to the degree of current LV filling impairment. We examined patients with acute coronary syndromes in sinus rhythm and without valvular disease (n = 154), and age- and gender-matched healthy controls (n=50) with echocardiography, applying pulsed Doppler international recommendations to group the patients according to the LV filling pattern: 0, normal; 1, delayed relaxation; 2, an isolated abnormal mitral pulmonary venous A-wave duration difference; 3, pseudonormal; and 4, restrictive. The LA and RA areas were measured in the 4-chamber view. Control values defined the normal range of: absolute LA area, LA area adjusted for body height, and LA-RA area. These areas indicated a LA enlargement in: (1) controls, 2%, 2%, and 4%, respectively; (2) patients with LV filling graded as normal/mildly impaired (groups 0 and 1), 15%, 17%, and 46%, respectively; moderately impaired (group 2), 26%, 29%, and 52%, respectively; and severely impaired (group 3 and 4), 42%, 38%, and 54%, respectively. Unequally sized atria appear to detect LA enlargement sensitively, especially when Doppler evidence of LV filling pathology is sparse. Clinically, with no obvious current cause for LA enlargement, a diagnosed "atrial size inequality" may still indicate a history of such causes.
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| 2. |
- Kashioulis, Pavlos, 1980, et al.
(författare)
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Adenine-Induced Chronic Renal Failure in Rats: A Model of Chronic Renocardiac Syndrome with Left Ventricular Diastolic Dysfunction but Preserved Ejection Fraction
- 2018
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Ingår i: Kidney & Blood Pressure Research. - : S. Karger AG. - 1420-4096 .- 1423-0143. ; 43:4, s. 1053-1064
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Tidskriftsartikel (refereegranskat)abstract
- Background/Aims: Cardiovascular disease is the major cause of death in patients with chronic kidney disease (CKD). Rats with adenine-induced chronic renal failure (ACRF) develop severe renal insufficiency and metabolic abnormalities that closely resemble those in patients with uremia. The aim of the present study was to determine left ventricular (LV) morphology and function in rats with ACRF. Methods: Male Sprague-Dawley rats received either chow containing adenine or were pair-fed an identical diet without adenine (controls, C). After 9-13 weeks animals were anesthetized with isoflurane and cardiac function was assessed both by echocardiography and by LV catheterization. Results: Rats with ACRF showed increases in serum creatinine (323 +/- 107 vs. 33 +/- 5 pM, P<0.05), mean arterial pressure (115 +/- 6 vs. 106 +/- 7 mmHg, P<0.05) and LV weight (3.4 +/- 0.3 vs. 2.5 +/- 0.2 mg/kg, P<0.05) vs. controls. Rats with ACRF had reduced early diastolic tissue Doppler velocities in the LV, enlarged left atrial diameter (4.8 +/- 0.8 vs. 3.5 +/- 0.4 mm, P<0.05) and elevated LV end-diastolic pressure (15 +/- 5 vs. 8 +/- 1 mmHg, P <0.01). Cardiac output was increased in ACRF rats (211 +/- 66 vs. 149 +/- 24 ml/min, P <0.05) and systolic function preserved. In the LV of ACRF rats there were statistically significant (P<0.05) increases in cardiomyocyte diameter, proliferation and apoptosis, while there was no difference between groups in fibrosis. Conclusion: Rats with ACRF develop LV hypertrophy and diastolic dysfunction while systolic performance was preserved. There was an increased hypertrophy and apoptosis of cardiomyocytes in the LV of ACRF rats. The cardiac abnormalities in ACRF rats resemble those in patients with CKD in which heart failure with preserved ejection fraction is common. Hence, this experimental model is well suited for studying pathophysiological mechanisms in chronic renocardiac syndromes. (C) 2018 The Author(s) Published by S. Karger AG, Basel
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| 3. |
- Kashioulis, Pavlos, 1980, et al.
(författare)
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Patients with moderate chronic kidney disease without heart disease have reduced coronary flow velocity reserve
- 2020
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Ingår i: ESC Heart Failure. - : Wiley. - 2055-5822. ; 7:5, s. 2797-2805
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Tidskriftsartikel (refereegranskat)abstract
- Aims The overall aim was to identify sub-clinical cardiac abnormalities by echocardiography in patients with chronic kidney disease (CKD) stages 3 and 4 and to investigate underlying mechanisms. Methods and results Ninety-one patients with CKD stages 3 and 4, without a diagnosis of heart disease, and 41 healthy matched controls were included in this cross-sectional study. Cardiac morphology and function were analysed with Doppler echocardiography and coronary flow velocity reserve (CFVR) in response to adenosine was measured in the left anterior descendent artery to detect coronary microvascular dysfunction (CMD). All study subjects had a left ventricular (LV) ejection fraction > 50%. Patients with CKD showed statistically significant increases in left atrial volume index and transmitral and pulmonary vein flow velocities during atrial contraction and prolonged LV isovolumetric relaxation time. Patients with CKD had significantly reduced CFVR vs. controls (2.74 +/- 0.86 vs. 3.40 +/- 0.89, P < 0.001), and 43% of patients were classified as having CMD compared with 9% of controls (P = 0.001). Conclusions Patients with CKD stages 3 and 4, without a diagnosis of heart disease, showed early abnormalities in LV diastolic function that did not fulfil the criteria for LV dysfunction according to current guidelines. A large proportion of CKD patients had CMD, suggesting that microvascular abnormalities may have a pathogenic role in the development of heart failure in this patient group.
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| 4. |
- Almodares, Qays, et al.
(författare)
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Larger right atrium than left atrium is associated with all-cause mortality in elderly patients with heart failure
- 2017
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Ingår i: Echocardiography - a Journal of Cardiovascular Ultrasound and Allied Techniques. - : Wiley. - 0742-2822. ; 34:5, s. 662-667
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundWhile left atrial (LA) enlargement is known as an early sign of left heart disease with prognostic implications in heart failure (HF), the importance of right atrial (RA) enlargement is less well studied, and the prognostic implications of interatrial size comparison are insufficiently understood. The aim of this study was to test the hypothesis that RA area larger than LA area in apical four-chamber view is associated with all-cause mortality in elderly patients with HF independent of left ventricular ejection fraction (LVEF). MethodsRetrospectively, 289 patients above 65years hospitalized for HF between April 2007 and April 2008, and who underwent an echocardiogram, were enrolled. All-cause mortality was registered during a follow-up of at least 56months. Baseline parameters measured were RA area, LA area, LA volume, LVEF, left ventricular mass (LVM), tissue Doppler systolic velocity of right ventricular free wall (SmRV), presence of severe tricuspid regurgitation (TR), tricuspid gradient, central venous pressure, systolic pulmonary artery pressure, as well as some parameters of diastolic function. ResultsIn univariate analysis RA larger than LA was associated with all-cause mortality (hazard ratio [HR] of 1.88, P<.001). The relation of RA larger than LA to all-cause mortality remained even after adjusting for age, heart rate, LVEF, atrial fibrillation, percutaneous coronary intervention, LVM index, LA volume index, SmRV, and the presence of severe TR (HR: 1.79, P=.04). ConclusionRA larger than LA, independently of LVEF, is associated with all-cause mortality in elderly patients hospitalized due to HF.
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| 5. |
- Collen, Anna-Clara, 1970, et al.
(författare)
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Cardiac structure and function is related to current blood pressure rather than to previous hypertensive pregnancy
- 2015
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Ingår i: Journal of Human Hypertension. - : Springer Science and Business Media LLC. - 0950-9240 .- 1476-5527. ; 29:11, s. 702-704
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Tidskriftsartikel (refereegranskat)abstract
- One-hundred five women were examined with echocardiography and ambulatory blood pressure measurements 40 years post partum to evaluate the effect of former hypertensive pregnancies versus current blood pressure on cardiac structure and function. Hypertensive pregnancies did not have an adverse effect on the heart, but current minor elevation in blood pressure had a negative impact on the myocardium. The increased prevalence of hypertension following hypertensive pregnancies may be a crucial factor regarding the increased risk for cardiovascular disease shown in affected women.
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| 6. |
- Glantz, Helena, et al.
(författare)
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Obstructive sleep apnea is independently associated with worse diastolic function in coronary artery disease
- 2015
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Ingår i: Sleep Medicine. - : Elsevier BV. - 1389-9457. ; 16:1, s. 160-167
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Tidskriftsartikel (refereegranskat)abstract
- Background: Diastolic dysfunction is common in patients with coronary artery disease (CAD). We hypothesize that patients with CAD and preserved left ventricular ejection fraction (LVEF) and obstructive sleep apnea (OSA) will have worse diastolic function than similar patients without OSA. Material and methods: We analyzed sleep-study recordings and echocardiographic measurements obtained at baseline in a randomized controlled trial (RICCADSA) of revascularized patients with CAD who had LVEF of at least 50%. OSA was defined as an apnea-hypopnea-index (AHI) >= 15 events/h, and, no OSA, as an AHI <5. Worse diastolic function was defined as assumed elevated left ventricular filling pressure based on peak flow velocity in early diastole/Tissue Doppler of early diastolic ventricular filling (E/e) of >13 (or >9 in patients with an enlarged left atrial diameter [>= 39 mm for women and >= 40 mm for men]). Results: Data from 431 patients were evaluated (mean age: 63.7 +/- 8.8 y; men: 82.5%; OSA: n = 331). Worse diastolic function was more common among the patients with OSA than those without (54.4% vs 41.0%, p = 0.019). In multivariate analysis, OSA was associated with worse diastolic function (odds ratio [OR] 1.90, 95% confidence interval [CI] 1.13; 3.18) adjusted for female sex (OR 2.28, 95% CI 1.28; 4.07), hypertension (OR 1.84, 95% CI 1.20; 2.82), and diabetes mellitus (OR 2.45, 95% CI 1.42; 4.23). Age >= 60 years, obesity, and current smoking were nonsignificant. Conclusions: In this cohort with CAD and preserved LVEF, OSA was associated with worse diastolic function independent of the traditionally recognized risk indicators. (C) 2014 Elsevier B.V. All rights reserved.
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| 7. |
- Guron, Cecilia Wallentin, 1965, et al.
(författare)
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Can the left ventricular early diastolic tissue-to-blood time interval be used to identify a normal pulmonary capillary wedge pressure?
- 2007
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Ingår i: Eur J Echocardiogr. - : Oxford University Press (OUP). - 1525-2167. ; 8:2, s. 94-101
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Tidskriftsartikel (refereegranskat)abstract
- The pulsed Doppler early diastolic left ventricular (LV) tissue (e)-blood (E) onset temporal relationship (e-E) is suggested to predict pulmonary capillary wedge pressure (PCWP), through the formulas: tau = 32 + 0.7(e-E) and PCWP = LV end-systolic pressure x e(-IVRT/tau). Small changes/errors in E could influence the quotient IVRT/tau by oppositely affecting IVRT and e-E. At rest in 50 healthy individuals we noted: e-E: 2 +/- 14 ms; IVRT: 89 +/- 17 ms; calculated tau: 33 +/- 10 ms; and PCWP: 9 +/- 9 mmHg (> 12 mmHg in 28%). Non-pharmacological preload alterations in 14 individuals rendered an intraindividual 'PCWP'-fluctuation of up to 40 mmHg. This application may therefore not be clinically robust.
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| 8. |
- Guron, Cecilia Wallentin, 1965
(författare)
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Pulsed Tissue Doppler and left ventricular filling in acute coronary syndromes
- 2005
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Pulsed tissue Doppler is a new technique, which can investigate longitudinal left ventricular(LV) function, by measuring tissue velocities and timings. Patients with acute coronarysyndromes (ACS) frequently display a reduced longitudinal function. They also developglobal LV filling impairment. This pathology involves an elevated LV filling pressure (FP),left atrial (LA) enlargement and elevation of right ventricular pressure (RVp). We aimed toinvestigate the relative timing of the onsets of the LV early diastolic longitudinal wall motionand blood flow, and further, to evaluate clinical tools to assess global LV filling.We studied 160 ACS patients and 60 controls with echocardiography, including pulsed tissueDoppler. Using pulsed blood pool Doppler, we semi-quantitatively classified the patients withrespect to LV filling: normal (group 0); delayed relaxation (group 1); isolated pathologicalmitral-pulmonary venous-A-wave-duration difference (group 2); pseudo normal (group 3); ora restrictive (group 4) filling pattern. The temporal onset relationship of the LV early diastolicwall lengthening (e) and the mitral inflow (E) was explored, for a regional wall analysis(paper I). In order to evaluate a recent application, suggested to predict pulmonary capillarywedge pressure (PCWP) through the formulas tau=32+0.7x (e-E) and PCWP = LV endsystolicpressure x e-IVRT/ tau (IVRT=the isovolumic relaxation time), we tested these formulasin normal individuals, at rest and during non-pharmacological preload alterations (Paper IV).The sensitivity of a new LV filling variable, the E/e (=E/E ) filling index was investigatedby comparing E/e to RVp in their identification of a Doppler-assumed elevated LVFP, i.e. apseudo normal or a restrictive filling pattern (Paper II). We compared the intraindividual atrialsize difference and absolute LA size, as detectors of LA enlargement (Paper III).In the patients, e started later than E (12±30 vs. 2±19 ms later, p<0.0001) and the intraindividualtime range was wider (43±27 vs. 30±18 ms, p<0.0001). In normal individuals atrest (n=50), the formula-calculated PCWP was 9±9 mmHg, exceeding 12 mmHg in 28 %.During altered preload (n=14), it showed an intraindividual fluctuation of up to 40 mmHg.An E/e filling index >15 and an RVp >30 mmHg had the following (%) sensitivity (32/94),specificity (95/76), positive (68/59), and negative (80/97) predictive value of a diagnosedgroup 3 or 4. Absolute LA area , LA area/body height and LA-right atrial area indicated aLA enlargement in; for controls: 2%, 2% and 4%; and for patients: group 0 and 1: 15%, 17%and 46%; group 2: 26%, 29% and 52%; and group 3 and 4: 42%, 38% and 54%.In ACS patients, the early diastolic LV tissue- to blood temporal relationship may reveal anasynchronous, and in relation to the mitral inflow delayed, initial LV wall lengthening.The formulas to predict PCWP failed to render plausible values in normal individuals. TheE/e filling index >15, as a single variable, may have a limited sensitivity of an elevated LVFP.An RVp of !30 mmHg could exclude a currently elevated LVFP. Atrial size inequality cansensitively detect LA enlargement, especially in only mildly impaired LV filling.
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| 9. |
- Guron, Cecilia Wallentin, 1965, et al.
(författare)
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The E/e filling index and right ventricular pressure in relation to applied international Doppler recommendations of left ventricular filling assessment
- 2005
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Ingår i: Eur J Echocardiogr. - : Oxford University Press (OUP). - 1525-2167. ; 6:6, s. 419-28
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Tidskriftsartikel (refereegranskat)abstract
- AIM: A ratio>15 between the early diastolic pulsed Doppler velocities of the mitral inflow (E) and the basal left ventricular (LV) tissue (e) has been demonstrated to predict an elevated LV filling pressure (FP). An elevated LVFP implies an elevated right ventricular pressure (RVp). In order to investigate the sensitivity of the E/e filling index, we compared E/e and RVp, in their ability to identify a Doppler-assumed elevation of LVFP. METHODS AND RESULTS: Application of pulsed Doppler international recommendations grouped 134 patients with acute coronary syndromes (ACS) and 50 age- and sex-matched controls, according to LV filling: normal; delayed relaxation; an isolated pathological mitral-pulmonary venous-A-wave-duration difference; pseudo normal; or a restrictive filling pattern. An E/e>15 and an RVp>30 mmHg showed the following (%) sensitivity (32/94), specificity (95/76), positive (68/59), and negative (80/97) predictive values of a Doppler-assumed elevation of LVFP, in terms of either a pseudo normal or a restrictive filling pattern. CONCLUSION: The low sensitivity of E/e to detect a Doppler-assumed elevation of LVFP could limit its clinical usefulness as a single variable, in ACS. The high sensitivity and negative predictive value of RVp support its use as an additional LV filling variable in these patients.
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| 10. |
- Guron, Cecilia Wallentin, 1965, et al.
(författare)
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Timing of regional left ventricular lengthening by pulsed tissue Doppler
- 2004
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Ingår i: J Am Soc Echocardiogr. - : Elsevier BV. - 0894-7317 .- 1097-6795. ; 17:4, s. 307-12
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Tidskriftsartikel (refereegranskat)abstract
- Pulsed tissue Doppler can measure myocardial velocities with high temporal resolution. Our aim was to determine the onset timing of the regional left ventricular longitudinal early lengthening (e) in relation to the mitral inflow (E) in acute coronary syndromes. We applied pulsed tissue Doppler to the septal, lateral, inferior, and anterior left ventricular basal walls of 160 patients with acute coronary syndromes and 60 control subjects. Maximum systolic and early diastolic velocities were lower for patient than for control walls (6.1 +/- 1.7 vs 7.9 +/- 1.4 cm/s, P <.0001, and 6.9 +/- 2.3 vs 10.0 +/- 2.3 cm/s, P <.0001, respectively) and e started later than E (12 +/- 30 vs 2 +/- 19 milliseconds later, P <.0001). All 3 variables related to the degree of visual left ventricular wall pathology. The intraindividual time range for all 4 e starts was wider for patients (43 +/- 27 vs 30 +/- 18 milliseconds, P <.0001). Our results show that pulsed tissue Doppler can identify a delayed and asynchronous initial wall lengthening in acute coronary syndromes.
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