Elsadig Kazzam

New concept in echocardiography: harmonic imaging of tissue without use of contrast agent

BACKGROUND Endocardial border detection is important for echocardiographic assessment of left-ventricular function. Second harmonic imaging of contrast agents enhances this border detection. We discovered that harmonic imaging improves tissue visualisation even before contrast injection. We therefore sought objectively to demonstrate the degree of enhancement of endocardial and myocardial visualisation. METHODS An ATL HDI-3000 scanner with software for contrast harmonic imaging was used to record short-axis images of the left ventricle in 27 patients with possible myocardial disease and 22 controls, in the fundamental mode and with harmonic imaging. A computer program measured the relative grey-scale values within six segments of the endocardium and myocardium. An Acuson Sequoia scanner equipped with software for tissue harmonic imaging was used to investigate the reproducibility of ejection-fraction calculations in 22 patients with ischaemic heart disease. FINDINGS Harmonic imaging produced brighter endocardium within each segment. Relative to the mean grey value of the total imaging sector, the values for harmonic and fundamental imaging were 171.5 vs 85.6% (p<0.0001) in end diastole and 194.1 vs 106.7% (p<0.0001) in end systole. Results for the myocardial segments were also significantly better for harmonic imaging. Structure enhancement of similar magnitude was seen among patients and healthy controls. Use of harmonic imaging reduced the proportion of unacceptable images by 14-46% in different views and improved the reproducibility of biplane ejection-fraction measurements. INTERPRETATION In comparison with fundamental imaging, the relative endocardial and myocardial brightness is enhanced by harmonic imaging.

Right ventricular outflow-tract fractional shortening: an applicable measure of right ventricular systolic function.

AIMS Assessment of right ventricular function is important. However, this is not easy to achieve due to the complex anatomy and geometry of the right ventricle, making the evaluation of its function limited. Therefore, a simple reliable and easy method is needed. This study was performed (1) to evaluate the use of right ventricular outflow tract fractional shortening obtained by M-mode echocardiography as a measure of right ventricular systolic function and (2) to determine the relationship between this parameter and other established measurements of right ventricular function such as long axis excursion. METHODS AND RESULTS Ninety-two consecutive patients referred for echocardiographic assessment of left and right ventricular function, age mean+/-SD was 68+/-14 years, were investigated. Twenty healthy controls, age 46+/-12 years were also studied. M-mode echocardiography was used to measure right ventricular outflow tract fractional shortening and right ventricular long axis excursion. Doppler echocardiography was used for the estimation of right ventricular-right atrial pressure drop and pulmonary artery acceleration time. Right ventricular outflow tract fractional shortening (P<0.0001), right ventricular long axis excursion (P<0.0001) and pulmonary acceleration time (P<0.0001) were reduced in patients compared to controls. Right ventricular outflow tract fractional shortening correlated with long axis excursion (r=0.66 P<0.0001), pulmonary artery acceleration time (r=0.80 P<0.0001) and right ventricular-right atrial pressure drop (r=-0.53 P<0.0001). Right ventricular long axis excursion correlated with right ventricular-right atrial pressure drop though to a lesser significance (r=-0.27 P <0.001). Furthermore, right ventricular outflow tract fractional shortening was reduced in patients with pulmonary hypertension compared to patients without, this difference was not observed in the right ventricular systolic long axis excursion. CONCLUSION Right ventricular outflow tract fractional shortening provides a simple and non-invasive measure of right ventricular systolic function. In combination with long axis excursion and Doppler velocities they should provide comprehensive assessment of right ventricular function.

Regional and Global Right Ventricular Function in Healthy Individuals Aged 20–90 Years: A Pulsed Doppler Tissue Imaging Study Umeå General Population Heart Study

The aim of the present study was to describe regional and global right ventricular (RV) function in a wide age range of healthy subjects of both sexes. We studied 255 (125 females) healthy individuals randomly selected from the Umeå General Population Register, age 58 ± 19 (range 22–89) years. RV function was studied using myocardial tissue Doppler imaging of the RV free wall. Isovolumic contraction (IVCv), systolic (Sv), early (Ev), and late (Av) diastolic velocities were measured. Furthermore, isovolumic periods and ejection time intervals were also measured. Conventional Doppler was used to study RV global filling properties. While systolic myocardial velocities were conserved over age, there was a decrease in myocardial E/A ratio with increasing age (r =−0.67, P < 0.001, for base) taken from the RV free wall. A similar age relation was found in RV global filling velocities with a reduced tricuspid E/A ratio (r =−0.57, P < 0.001). Furthermore, a significant correlation was found between global and regional E/A ratios at the basal (r = 0.58, P ≤ 0.001) and mid‐segmental levels (r = 0.46, P ≤ 0.001). Systolic myocardial velocities behaved independent of age whereas regional as well as global E/A ratio were age‐related. No relationship was found between regional isovolumic time intervals and age. Knowledge of these age‐dependent relationships is fundamental when evaluating RV function in patients.

Correlation between increased nitric oxide production and markers of endothelial activation in systemic sclerosis: Findings with the soluble adhesion molecules E‐selectin, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1

OBJECTIVE To determine the relationship between vascular function and the inflammatory response in systemic sclerosis (SSc), and to investigate whether production of endothelial-derived nitric oxide (NO) is disturbed in this disease. METHODS We measured plasma nitrate, urinary excretion of both nitrate and cGMP, and soluble adhesion molecules of endothelial origin in patients with SSc and in age- and sex-matched controls and compared these levels between groups. Additionally, we performed correlation analysis to determine how these variables were related to one another. Plasma nitrate and 24-hour-urinary excretion of nitrate in patients and controls were measured after a 72-hour nitrate-free-diet, using a gas chromatography/mass spectrometric method. Soluble adhesion molecules intercellular adhesion molecule 1 (sICAM-1), vascular cell adhesion molecule 1 (sVCAM-1), and E-selectin and cytokines were measured by enzyme-linked immunosorbent assay. The expression of E-selectin was further investigated in skin biopsy specimens by immunoperoxidase staining, and the presence of inducible NO synthase by immunoblotting. RESULTS Plasma nitrate and 24-hour-urinary-excretion of cGMP were significantly elevated in patients compared with controls, while 24-hour-urinary-excretion of nitrate tended to be elevated in SSc patients. Levels of sICAM-1, sVCAM-1, and sE-selectin were significantly elevated in the patients. Levels of plasma nitrate in the patients correlated significantly with levels of sVCAM-1 (P = 0.020) and sE-selectin (P = 0.018) and approached a significant correlation with sICAM-1 (P = 0.055), suggesting that activated endothelial cells may produce plasma nitrate. CONCLUSION NO synthesis is elevated in SSc patients, and the activated endothelial cell is a likely site of its production.

Identification of the genotypes causing hypertrophic cardiomyopathy in northern Sweden

Hypertrophic cardiomyopathy (HCM) is a heterogenous disease, with variable genotypic and phenotypic expressions, often caused by mutations in sarcomeric protein genes. The aim of this study was to identify the genotypes and associated phenotypes related to HCM in northern Sweden. In 46 unrelated individuals with familial or sporadic HCM, mutation analysis of eight sarcomeric protein genes was performed; the cardiac beta-myosin heavy chain, cardiac myosin-binding protein C, cardiac troponin T, alpha-tropomyosin, cardiac essential and regulatory myosin light chains, cardiac troponin I and cardiac alpha-actin. A total of 11 mutations, of which six were novel ones, were found in 13 individuals. Seven mutations were located in the myosin-binding protein C gene, two in the beta-myosin heavy chain gene and one in the regulatory myosin light chain and troponin I genes, respectively. This is the first Swedish study, where a population with HCM has been genotyped. Mutations in the cardiac myosin-binding protein C gene were the most common ones found in northern Sweden, whereas mutations in the beta-myosin heavy chain gene were less frequent than previously described. There are differences in the phenotypes mediated by these genes characterised by a more late-onset disease for the myosin-binding protein C gene mutations. This should be taken into consideration, when evaluating clinical findings in the diagnosis of the disease, especially in young adults in families with HCM, where penetrance can be expected to be incomplete in the presence of a myosin-binding protein C gene mutation.

COLD-INDUCED REVERSIBLE MYOCARDIAL ISCHAEMIA IN SYSTEMIC SCLEROSIS

The effect of cold provocation on myocardial perfusion was studied in 21 patients with systemic sclerosis and 8 healthy controls. The cold provocation was designed not to cause a pain reaction, and no rise in heart rate/blood pressure product occurred during provocation. Myocardial perfusion was assessed by measurement of thallium uptake by imaged single photon emission computed tomography. No patient had clinical evidence of cardiac involvement, but abnormal electrocardiographic (ECG) findings were found in 5. In 12 patients cold-induced reversible perfusion defects were found; 9 of these also had permanent defects. A further 3 patients had permanent perfusion defects but no reversible defects. The permanent and/or reversible perfusion defects were not related to age among the patients and were not seen in any of the healthy controls, whose age distribution was similar. The reversible and permanent defects were not related to other features of systemic sclerosis, nor to the ECG findings. It is concluded that abnormalities in myocardial perfusion are common in systemic sclerosis and may be present without apparent clinical myocardial involvement. A cold-induced vasopastic process in the myocardial circulation might contribute to the development of the patchy myocardial fibrosis seen in patients with systemic sclerosis.

Contrasting actions of diesel exhaust particles on the pulmonary and cardiovascular systems and the effects of thymoquinone

BACKGROUND AND PURPOSE Acute exposure to particulate air pollution has been linked to acute cardiopulmonary events, but the underlying mechanisms are uncertain.

Evaluation of the direct systemic and cardiopulmonary effects of diesel particles in spontaneously hypertensive rats.

Recent data suggest that ultrafine pollutant particles (diameter <0.1microm) may pass from the lung into the systemic circulation. However, the systemic and cardiorespiratory effects of translocated particles are not well known. In this study, we determined the direct acute (24h) effect of the systemic administration of 0.01mg/kg and 0.02mg/kg diesel exhaust particles (DEP) on systolic blood pressure, heart rate, and both systemic and pulmonary inflammation in spontaneously hypertensive rats (SHR). Compared to the blood pressure in control group, rats exposed to DEP exhibited a dose-dependent increase in systolic blood pressure, at 0.01mg/kg (P<0.05) and 0.02mg/kg (P<0.01). Likewise, the heart rate was also dose-dependently increased at 0.01mg/kg (P:NS) and 0.02mg/kg (P<0.01) compared to control SHR. DEP exposure (0.02mg/kg) significantly elevated the number of leukocytes in blood (P<0.05), interleukin-6 (IL-6, P<0.005), tumor necrosis factor alpha (P<0.05) and leukotriene B4 (LTB4, P<0.005) concentrations in plasma. Moreover, in SHR given 0.02mg/kg, the number of platelet was significantly reduced (P<0.05), whereas the tail bleeding time was prolonged (P<0.05). Pulmonary inflammations were confirmed by the presence of a significant increase in the number of macrophages (0.02mg/kg) and neutrophils (0.01 and 0.02mg/kg) and protein contents (0.02mg/kg) in bronchoalveolar lavage (BAL) compared to saline-treated SHR. Also, IL-6 (0.01mg/kg; P<0.05 and 0.02mg/kg; P<0.01), LTB4 (0.02mg/kg; P<0.05) concentrations in BAL and the superoxide dismutase activity (0.02mg/kg; P=0.01) were significantly elevated compared to control group. We conclude that, in SHR, the presence of DEP in the systemic circulation leads not only to cardiac and systemic changes, but also triggers pulmonary inflammatory reaction involving IL-6, LTB4 and oxidative stress.

Amyloid heart disease mimicking hypertrophic cardiomyopathy

Objective.  To investigate the importance of transthyretin (TTR) gene mutations in explaining the phenotypic expression in patients diagnosed with hypertrophic cardiomyopathy (HCM) in northern Sweden.

Non‐invasive assessment of left ventricular diastolic function in patients with systemic sclerosis

Abstract. To evaluate the extent of left ventricular (LV) diastolic impairment in systemic sclerosis, we examined 30 consecutive patients (15 men and 15 women) with this condition, and compared the findings with the data for 48 age‐ and sex‐matched randomly sampled controls. All patients were investigated by phonocardiography, pulse curve recording, and M‐mode echocardiography. Twenty‐three of 30 (77%) patients had LV hypertrophy and/or diastolic impairment. Interventricular septum (P= 0.0001), LV posterior wall (P< 0.05), and the wall thickness to cavity dimension ratio (P< 0.001) were increased in patients compared to controls, as was LV mass index (P< 0.002). Five patients had asymmetric septal hypertrophy. LV end‐diastolic dimension did not differ between groups. LV distensibility was impaired, as judged from apexcardiographic a/H ratio (P< 0.05) and from an increased left atrial index (P< 0.005). LV early filling was impaired, with a reduced left atrial emptying index (P= 0.0001), and a reduced rate of dimension increase in digitized M‐mode (P< 0.02). We found no evidence of impaired LV relaxation. Blood pressure did not differ between patients and controls. With longer duration of the disease, left atrial dimension appeared to increase (r = 0.42, P< 0.05), while other variables were not related to disease duration. The impaired LV filling was not secondary to systolic dysfunction. We conclude that systemic sclerosis patients have an increased LV wall thickness, with impaired early filling properties and LV distensibility.