Lower Systolic Velocity Research Articles

Дослідження центральної та периферичної гемодинаміки в дітей із септичним шоком за допомогою ехокардіографії та ультразвукової допплерографії

Актуальність. Тяжкий перебіг сепсису зазвичай асоціюється з розвитком септичного шоку та поліорганної недостатності. Для ефективного лікування рекомендується проводити інструментальний контроль за показниками переднавантаження, скоротливої здатності серця та перфузії тканин. Мета дослідження — вивчення змін центральної та периферичної гемодинаміки за допомогою ехокардіографії та ультразвукової допплерографії в дітей із септичним шоком. Матеріали та методи. Проведено ретроспективне дослідження випадків септичного шоку в дітей віком від 0 до 18 років, які проходили лікування у відділенні інтенсивної терапії. Хворим здійснювався моніторинг центральної та периферичної гемодинаміки за допомогою ехокардіографії та ультразвукової допплерографії. Результати. Було досліджено 34 випадки сепсису, що асоціювався із септичним шоком. У 24 (70,6 %) хворих етіологічним фактором був менінгокок, у 1 (2,9 %) — стафілокок, у 9 (26,5 %) — етіологію не було встановлено. У 6 дітей із досліджуваної групи захворювання закінчилось летально. У гострому періоді шоку середні показники артеріального тиску, фракції викиду, периферичного опору, діастолічної швидкості в абдомінальній аорті та верхній брижовій артерії були відносно зниженими і зростали після стабілізації гемодинаміки. Фатальний перебіг захворювання асоціювався з високими показниками частоти серцевих скорочень, нижчими показниками максимальної швидкості в черевному стовбурі та стегновій артерії, діастолічної швидкості та показником периферичного опору у нирковій артерії при ініціальному обстеженні. Висновки. Комплексне дослідження показників центральної та регіонарної гемодинаміки в дітей за допомогою ехокардіографії та ультразвукової допплерографії дозволяє проводити неінвазивну діагностику ранніх порушень, пов’язаних із септичним шоком, та здійснювати контроль ефективності терапевтичних заходів.

Electromechanical Relationship in Hypertrophic Cardiomyopathy

We examined whether there is a relationship between repolarization abnormalities on electrocardiography (EKG) and deformation abnormalities by echocardiography. Analysis of baseline EKGs and mechanical (echo-based deformation) changes was performed in 128 patients with a clinical diagnosis of hypertrophic cardiomyopathy (HCM). Patients with left ventricular hypertrophy (LVH) or repolarization abnormalities had higher septal thickness when compared to patients with normal EKG. Patients with EKG evidence of LVH or QTc prolongation had lower systolic velocity, systolic strain, systolic strain rate, late diastolic velocity, and late diastolic strain rate than patients with a normal EKG. Patients with strain pattern or ST depression/T-wave inversion had lower systolic velocity, systolic strain, systolic strain rate, early diastolic velocity, and late diastolic velocity when compared to patients with normal EKGs. LVH and repolarization abnormalities on surface EKG are markers of impaired systolic and diastolic mechanics in HCM.

Additive Compensatory Effects of Cardiac Troponin I and Cardiac Troponin T N-Terminal Truncations on the Disease Phenotypes of a Familial Hypertrophic Cardiomyopathy Mutation (E180G) of α-Tropomyosin

A naturally occurring proteolytic N-terminal truncation of cardiac troponin I (cTnI-ND) has been shown to compensate for functional abnormalities caused by cardiomyopathic mutations. A proteolytic N-terminal truncation of cardiac TnT (cTnT-ND) elongates ventricular ejection time to compensate for cardiac output against high pressure load. To investigate the mechanisms for these troponin modifications to modulate the function of cardiac muscle thin filament, we produced transgenic mouse lines co-expressing cTnI-ND and/or cTnT-ND with a family hypertrophic cardiomyopathy mutation of cardiac α-tropomyosin (TM-E180G). The over expression of TM-E180G resulted in ∼90% replacement of endogenous α-tropomyosin in the cardiac muscle with normal total stoichiometry. Functional studies in ex vivo working hearts of 2-month-old TM-E180G mice showed lower diastolic velocity and higher left ventricular diastolic pressure, indicating higher Ca2+ sensitivity. β-MHC expression together with myocardial fibrosis was found in the left ventricle of 28-day and 2-month-old TM-E180G mice with early failing phenotypes (lower stroke volume and lower systolic velocity). In double and triple transgenic mouse hearts, expression of cTnI-ND and/or cTnT-ND decreased the occurrence of β-MHC in TM-E180G mouse hearts. Functional studies showed cTnI-ND+cTnT-ND did not override the contractile phenotype of TM E180G mutation but had beneficial effects on improving stroke volume and reducing fibrosis, with additive effects in the triple transgenic hearts. While TM-E180G mice usually die between 4 and 5 months of age, cardiac function of TM-E180G+cTnI-ND+cTnT-ND triple transgenic mice remained apparently normal at 10-11 months of age as shown by the compensated heart function and cardiac efficiency with minimal β-MHC occurrence. These results demonstrated compensatory effects of posttranslational modifications of troponin on the functional abnormality of tropomyosin for potential applications in the treatment of heart failure.

Arterial flow characteristics in the presence of vascular disease and implications for fast spin echo‐based noncontrast MR angiography

To investigate arterial flow characteristics in the setting of vascular disease, and examine their effect on the performance of fast spin-echo (FSE)-based noncontrast MR angiography (NC-MRA). Seventeen patients were recruited from among those scheduled for routine contrast-enhanced MR angiography (CE-MRA) of the lower extremities at 1.5 Tesla. The research portion of the exam was performed before the clinically-indicated protocol and included phase-contrast imaging at multiple levels in the legs and FSE-based NC-MRA in the calf and thigh, using a three-dimensional ECG-gated technique that exploits differences in arterial flow velocity between diastole and systole. Vascular occlusions were associated with reduced systolic velocity, a delayed systolic peak, and, in two middle-aged patients, an increase in diastolic velocity. Elevated systolic and diastolic velocities were observed in a subject with a nonhealing ulcer. NC-MRA allowed visualization of arteries with systolic velocities as low as 3 cm/s, and exhibited comparable depiction to CE-MRA for diastolic velocities as high as 6 cm/s. At the highest diastolic velocities observed (15 cm/s) arterial depiction was severely degraded. FSE-based NC-MRA as presently implemented performs successfully over a wide range of flow patterns, but does not accommodate extremely low systolic velocities or very high diastolic velocities.

Impaired Diastolic Function and Disruption of the Force-Frequency Relationship in the Right Ventricle of Newborn Pigs Resuscitated with 100% Oxygen

Background: Resuscitation with 100% oxygen increases oxidative stress and is detrimental for organ function. Objective: To study the effects of resuscitation with 100% oxygen compared to room-air on myocardial function. Methods: Twenty-eight newborn pigs underwent global hypoxia (8% oxygen/N₂) until base excess reached –20 mmol/l. The animals were randomized into two groups and resuscitated with either 100% or room air for 30 min. Myocardial tissue Doppler velocities and acceleration of the mitral and tricuspid valve annuli during systole and diastole were assessed before global hypoxia and after resuscitation together with troponin I. Results: Peak early diastolic velocity (E′) and acceleration (pEac) in the septum and pEac in the lateral tricuspid valve annulus were lower after resuscitation with 100% oxygen, suggesting impaired diastolic relaxation in the right ventricle. Lower systolic velocities and acceleration in the right ventricle relative to heart rate indicate disruption of the right ventricular force-frequency relationship after resuscitation with 100% oxygen. Troponins were higher in the 100% oxygen group, suggesting increased myocardial damage in this group. Conclusion: Resuscitation with 100% oxygen compared to room air induces diastolic dysfunction, disrupts the systolic force-frequency relationship and increases myocardial damage in the newborn pig.

Echocardiographic epidemiology--an emerging tool for early diagnosis, studying pathophysiology, predicting prognosis, and testing treatments

Advances in echocardiography mean that it is now possible to measure myocardial function accurately and non-invasively. Paradoxically, objective quantification of myocardial motion, contraction, and relaxation in each segment of the left ventricle actually makes it more difficult to define normality and disease in the individual patient, but the technique raises intriguing possibilities in population studies for diagnosing early heart muscle disease and testing new approaches to treatment. The catalyst to this approach was the development of tissue Doppler echocardiography to measure the velocity of myocardial motion, and then the processing of digitally stored velocity data to obtain measurements of regional myocardial deformation (strain and strain rate). Machines do not apply the Doppler equation when processing these signals, and so an alternative and more accurate term that encompasses all available methods is myocardial velocity imaging. Mogelvang et al. have reported their findings from performing echocardiography in >1000 subjects in the Copenhagen City Heart Study.1 These subjects comprised 17% of the total sample which had been drawn randomly from population registers, who attended when echocardiography with myocardial velocity imaging could be performed. They were aged between 20 and 93 years, and included substantial numbers of subjects with hypertension (>140/90 mmHg), diabetes [plasma glucose >11.1 mmol/L, or glycosylated haemoglobin (HbA1c) >7%, or on treatment], and/or ischaemic heart disease (IHD, diagnosed from history or abnormal ECG). Compared with ‘control’ subjects with none of these conditions, the subjects with hypertension, diabetes, or IHD had lower systolic velocities of long-axis shortening of the left ventricle (on average, –13%), less systolic mitral annular excursion (also –13%), and lower velocities of long-axis lengthening in early diastole (by an average of –33%). Overall, only 2% of the subjects with disease had a low ejection fraction (<50%) and only 8% had any degree of … *Corresponding author. Tel: + 44 29 2074 3489, Fax: + 44 29 2074 3500, Email: fraserag{at}cf.ac.uk

Coronary microvascular dysfunction in patients with symptomatic hypertrophic cardiomyopathy

Background: Patients with hypertrophic cardiomyopathy (HCM) have been shown to have reduced myocardial perfusion in the presence of normal epicardial arteries. The mechanism of abnormal microvascular function is not well understood. Hypothesis: A possible mechanism for the reduction in CFR may be that the microcirculation is already near maximal dilation in the basal state and is therefore limited in the ability to further dilate and compensate for the increase in myocardial demand. Methods: Eight patients with symptomatic HCM and eight age- and sex-matched controls were studied. All patients underwent coronary angiography and coronary hemodynamic assessment with an intracoronary Doppler wire to determine total coronary blood flow, coronary resistance, and coronary flow reserve (CFR). Phasic blood flow parameters were also obtained. Results: Compared with controls (n = 8), patients with HCM (n = 8) had higher coronary blood flow (52±19 versus 33±11 mL/min, P = 0.03), lower coronary resistance (2.12±0.91 versus 3.13±0.93 mm Hg/mL/min, P = 0.05), and lower CFR (2.1±0.7 versus 3.4±1.0 mm, P = 0.02). There was a direct correlation between CFR and coronary resistance (r = .5, P = .05). HCM patients also had abnormal phasic coronary flow characteristics with lower systolic velocities or reversal of flow during systole, and a more rapid deceleration of diastolic blood flow (40.7±13.2 versus 27.5±8.5 cm/sec2, P=.03). Conclusion: The reduction of CFR in HCM patients may be secondary to near maximal vasodilatation of the microcirculation in the basal state rather than narrowing of intramyocardial small arteries. Symptomatic HCM patients also have abnormal phasic coronary blood flow with a greater dependence on diastolic flow and a more rapid deceleration of diastolic blood flow.

Doppler evaluation of renal blood flow velocity as a predictive index of acute renal failure in perinatal asphyxia.

Aim of our study was to evaluate Doppler renal blood flow velocity in asphyxiated neonates and to correlate renal function to Doppler findings. Doppler renal blood flow velocity was evaluated in 23 severely asphyxiated neonates born at a gestational age > 32 weeks and compared to our standard Doppler data obtained in 25 healthy neonates comparable for gestational age and birth weight. Renal Doppler ultrasound was performed on the 1st and 3rd days of life. Renal function was investigated in the first 2 weeks of life. Asphyxiated neonates showed mean values of systolic velocity and mean velocity significantly reduced (P < 0.001) compared with our standard Doppler values on the 1st day of life. Seven out of the 23 asphyxiated neonates were affected by acute renal failure and 14 showed no renal involvement. Two neonates were oliguric but did not develop acute renal failure. On the 1st day of life, neonates with acute renal failure had significantly lower mean values of systolic velocity and mean velocity than the asphyxiated neonates without renal involvement (P < 0.01). All 7 neonates affected by acute renal failure showed a systolic velocity more than 2SD below the mean standard value, while only 4 of the 16 asphyxiated neonates (25%) without acute renal failure had low systolic velocity values on the 1st day of life. Doppler velocities in asphyxiated neonates were similar to standard values on the 3rd day of life. Renal failure recovered before the 11th day of life in all cases. Our findings indicate that decreased Doppler renal flow systolic velocity observed in asphyxiated neonates on the st day of life is a useful predictive index for subsequent development of acute renal failure, with 100% sensitivity and 63.6% specificity.

Atrial and ventricular function after cardioversion of atrial fibrillation.

Previous studies on atrial recovery after cardioversion of atrial fibrillation have not taken into account new knowledge about the pathophysiology of transmitral and transtricuspid flow velocity patterns. It is possible to shed further light on this problem if atrioventricular inflow velocity, venous filling pattern, and atrioventricular annulus motion are recorded and interpreted together. Prospective examinations of mitral and tricuspid transvalvar flow velocities, superior caval and pulmonary venous filling, and mitral and tricuspid annulus motion were recorded using Doppler echocardiography. Examinations were performed before and 24 hours, 1 month, and 20 months after cardioversion. Tertiary referral centre for cardiac disease with facilities for invasive and non-invasive investigation. 16 patients undergoing cardioversion of atrial fibrillation in whom sinus rhythm had persisted for 24 hours or more. Before conversion there was no identifiable A wave in transvalvar flow recordings. The total motion of the tricuspid and mitral annulus was subnormal and there was no identifiable atrial component. Venous flow patterns in general showed a low systolic velocity. After conversion, A waves and atrial components were seen in all patients and increased significantly (P < 0.01) with time. There was a similar time course for the amplitude of annulus atrial components, an increased systolic component of venous inflow, an increased A wave velocity, and a decreased E/A ratio of the transvalvar velocity curves. The ventricular component of annulus motion was unchanged. Changes in general occurred earlier on the right side than the left. This study indicates that, in addition to the previously known electromechanical dissociation of atrial recovery that exists after cardioversion of atrial fibrillation, there may also be a transient deterioration of ventricular function modulating the transvalvar inflow velocity recordings. Function on the right side generally becomes normal earlier than on the left. Integration of information from transvalvar inflow curves, annulus motion, and venous filling patterns gives additional insight into cardiac function.