Biomedical subjects

M Y Henein

Publications and source records attributed to M Y Henein.

10 recordsLinked to original sources

PubMed1997

Asynchronous left ventricular wall motion in unstable angina.

The objective of the study was to assess the nature of left ventricular wall motion disturbances in patients with unstable angina and the relative contributions of the severity of symptoms and the severity of coronary artery disease (CAD) to their genesis. A prospective examination was performed on 30 patients with unstable angina (UA) with triple CAD, 34 matched patients with chronic stable angina (CSA) (20 with triple CAD and 14 with isolated left anterior descending (LAD) artery disease), and compared to 21 normals. LV cavity size was normal in all three groups. Twenty-two of 30 patients with UA had marked (>3 mm) abnormal long axis shortening during isovolumic relaxation time (IVRT), 65% of LV sites being abnormal. In CSA, minor (<3 mm) shortening during IVRT occurred in 7 patients with triple CAD, and in 5 with LAD disease, with 12% of LV sites involved in both groups, P<0.001 vs. UA. The incidence of other long axis abnormalities, including reduced extent and peak rate of shortening and lengthening as well as the delay in the onset of shortening and lengthening was increased between patients with CSA and triple CAD compared with LAD but not between the two groups of patients with triple CAD, CSA and UA. Transmitral E/A ratio was also reduced in the two groups with triple vessel disease, CSA and UA. Thus, the incidence of minor long axis abnormalities is similar in CSA and UA and is related to the severity of CAD. However, abnormal shortening during IVRT is more severe and generalised in UA but not in CSA with triple vessel disease. We suggest that these abnormalities of wall motion bear a close relation to the development of instability within the setting of CAD.

Aged↗

PubMed1997

Effects of acute coronary occlusion and previous ischaemic injury on left ventricular wall motion in humans.

OBJECTIVE: To assess the acute effects of single and repeated coronary artery occlusions, during percutaneous transluminal coronary angioplasty (PTCA), on left ventricular long axis function in patients with stable and unstable angina. DESIGN: Prospective examination of ventricular systolic and diastolic long axis function using M mode echocardiography and transmitral Doppler in patients with significant coronary artery stenosis and either stable or unstable angina, during routine PTCA. SETTING: A tertiary referral centre for heart disease with cardiac catheterisation and echocardiographic facilities. SUBJECTS: 36 patients, age (SD) 60 (8) years, with significant coronary artery disease undergoing PTCA (mean duration 100-130 seconds) to the left anterior descending coronary artery (LAD) in 18 patients, native LAD or its vein graft in eight, and right coronary artery in 10. Controls were 21 normal subjects, age 58 (11) years. RESULTS-AT BASELINE: in systole, total long axis excursion was reduced at septal, posterior, and right sites in patients with LAD disease, at right site in those with vein grafts, and at septal and right sites in patients with right coronary artery disease. Peak shortening rate was often reduced in all patients and onset of shortening delayed with respect to the Q wave in patients with LAD disease. In diastole, onset of lengthening was always delayed, peak lengthening rate reduced, and relative A wave amplitude increased in all patients. There was a consistent abnormal shortening of the long axis during the isovolumic relaxation period in the 14 patients with unstable angina, not seen in the others. Transmitral A wave velocity was also increased and the onset of E wave delayed with respect to A2. At first balloon inflation: the extent of pre-existing systolic and particularly diastolic abnormalities consistently increased in patients with LAD or right coronary artery occlusion. This was associated with further delay in the onset of the transmitral Doppler E wave as its peak velocity fell and E/A ratio increased. In unstable angina, balloon inflation caused minor changes only in systolic function and no change in diastolic function. At second balloon inflation: systolic changes were the same as with the first inflation, while diastolic changes were attenuated by 10-15%. CONCLUSIONS: In stable angina intracoronary balloon inflation aggravated pre-existing systolic and diastolic abnormalities in the territory of the occluded vessel, indicating the dependence of both on coronary flow. In unstable angina balloon inflation caused only minor deterioration in systolic function, and diastolic changes-including the characteristic abnormal shortening during isovolumic relaxation-were unaffected. Thus resting abnormalities of left ventricular function in unstable angina are effectively dissociated from acute changes in coronary flow. Overall, the severity of systolic disturbances was unaltered by a second balloon inflation, but diastolic disturbances were attenuated by 10-15%, compatible with ischaemic preconditioning or recruitment of collaterals.

Aged↗

PubMed1996

Effect of acute alterations in afterload on left ventricular function in patients with combined coronary artery and peripheral vascular disease.

OBJECTIVE: To assess the effect of acute alterations in afterload by aortoiliac clamping, during peripheral vascular surgery, on left ventricular function. DESIGN: Prospective examination of the left ventricular long axis and transmitral Doppler flow preoperatively and intraoperatively; before aortic clamping, during clamping and 5 min, 15 min, and 5 days after unclamping. SETTING: A tertiary referral centre for cardiac and vascular disease equipped with invasive and non-invasive facilities. PATIENTS: 20 patients (11 men; mean (SD) age 61 (8) years) with significant aortoiliac disease and documented coronary artery disease and 21 normal controls of similar age. RESULTS: Preoperatively: long axis function was abnormal compared with that in normal controls. In systole total long axis excursion and peak shortening rate were reduced, onset of shortening delayed, and there was pre-ejection lengthening (P < 0.001). In diastole there was abnormal shortening during isovolumic relaxation, delaying the onset of long axis lengthening (P < 0.001). Peak lengthening rate was also reduced and A wave excursion increased (P < 0.001). Transmitral Doppler showed increased A wave velocity and reduced peak E/A diastolic flow velocities ratio (P < 0.001). Intraoperatively: preclamping results did not differ from those before operation. With clamping the extent of systolic and diastolic abnormalities promptly increased as to a lesser extent did those of transmitral flow velocity, although heart rate and blood pressure did not change significantly. Total long axis excursion and A wave amplitude were more reduced by aortic than iliac clamping, whereas the onset of lengthening was more delayed and the lengthening velocity more reduced with iliac clamping. Some 5 min after unclamping systolic long axis function had already returned towards normal; total excursion increased, as did the peak shortening rate, and the onset of shortening became less delayed (P < 0.001). In diastole the delayed onset of lengthening regressed, its lengthening velocity increased, and A wave excursion fell (P < 0.001). Early diastolic transmitral flow velocity also increased. This improvement in systolic and diastolic long axis function had progressed 15 min after unclamping but showed no further change at 5 days. At 5 days after operation, however, systolic and diastolic measurements had improved compared with those preoperatively. CONCLUSION: Resting left ventricular long axis function is abnormal in patients with combined coronary artery disease and peripheral vascular disease. It is unaffected by anaesthesia but deteriorates with aortic or iliac clamping, although blood pressure remains unchanged. It promptly improves with unclamping after successful peripheral arterial reconstruction. Thus, even in apparently stable coronary artery disease, resting subendocardial function is labile, showing pronounced alterations with changing after-load, even when arterial pressure itself does not change.

Blood Pressure↗

PubMed1996

ACE inhibitors unmask incoordinate diastolic wall motion in restrictive left ventricular disease.

OBJECTIVE: To assess the effect of ACE-inhibition on left ventricular filling and wall motion in patients with a clinical diagnosis of heart failure. DESIGN: Prospective examination of left ventricular systolic and diastolic function using M mode echocardiography and pulsed and continuous wave Doppler before and three weeks after starting an ACE inhibitor. SETTING: A tertiary referral centre for cardiac disease equipped with non-invasive facilities. SUBJECTS: 30 outpatients with a clinical diagnosis of heart failure in whom treatment with an ACE inhibitor was started; age 61 (SD 11) years; 27 male; 3 female; 21 healthy controls of similar age. RESULTS: Left ventricular cavity was dilated both at end systole and end diastole, and fractional shortening reduced. Although mean isovolumetric relaxation time (IVRT) and transmitral E (early) to A (late) filling velocity (E/A) ratio were not different from normal, a value of 1.0 on the normal frequency plot of the E/A ratio divided the patients bimodally into two groups: 20 patients (group A) with E/A ratio > 1.0 and 10 patients (group B) < 1.0. In group A patients, IVRT was short as was transmitral E wave deceleration time compared to normal (P < 0.001), fulfilling the criteria of restrictive left ventricular physiology. Left ventricular wall motion during IVRT was coordinate and left ventricular end diastolic pressure was raised on the apex-cardiogram (P < 0.001). In group B, E wave deceleration time was longer, relaxation incoordinate, and apexcardiogram normal. With an ACE inhibitor: in group A, left ventricular dimensions fell at end diastole (P < 0.05) and end systole (P < 0.01) but fractional shortening did not change; long axis total excursion (P < 0.01) and peak rate of shortening (P < 0.05) both increased; IVRT increased (P < 0.001) with the appearance of markedly incoordinate wall motion, minor axis lengthening, and long axis shortening (P < 0.001 for both); A wave amplitude also consistently increased (P < 0.001); finally, transmitral E wave velocity fell and A wave velocity increased. ACE inhibition did not alter any of the left ventricular minor and long axis or transmitral Doppler variables in patients in group B. CONCLUSIONS: Patients with a clinical diagnosis of heart failure differ in their presentation and response to ACE inhibition according to baseline haemodynamics. In restrictive left ventricular physiology, ACE inhibition reduces cavity size and prolongs IVRT, compatible with a fall in left atrial pressure. At the same time, ventricular relaxation becomes very delayed and incoordinate, greatly reducing early diastolic left ventricular filling velocity. Thus ACE inhibition unmasks major diastolic abnormalities in patients with restrictive left ventricular disease.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1995

Suppression of left ventricular early diastolic filling by long axis asynchrony.

OBJECTIVE: To assess how early diastolic transmitral flow is suppressed in a group of patients in whom effective ventricular filling occurred exclusively with atrial systole. DESIGN: Prospective examination of the left ventricular transverse and longitudinal axes and transmitral Doppler flow. SETTING: A tertiary referral centre for cardiac diseases. SUBJECTS: 20 patients (mean (SD) age 65 (10) years) with isolated transmitral late diastolic flow were studied. None had sinus tachycardia, prolonged PR interval or a summation flow pattern. 21 normal individuals of similar age served as controls. RESULTS: The left ventricle was usually dilated, end diastolic diameter (6.6 (1.0) v 4.9 (0.5) cm, P < 0.001) and end systolic diameter (5.4 (1.1) v 3.3 (0.5) cm, P < 0.001) were both increased, and fractional shortening of the minor axis reduced (16 (7)% v 30 (10)%, P < 0.001) in patients in whom left ventricular early diastolic filling was absent compared with those of normal controls. Mitral valve opening was late after aortic valve closure (A2) (115 (30) v 60 (10) ms, P < 0.001). The minor axis increased during this period (30 (20)% v 8.6 (2.5)%, P < 0.001). Onset of detectable transmitral flow was further delayed after cusp separation (85 (25) v 25 (10) ms, P < 0.001). Left ventricular long axis function was very abnormal. Onset of shortening was delayed with respect to the q wave at the left and septal sites (150 (40) v 90 (20) ms and 145 (30) v 80 (10) ms respectively, P < 0.001) and major shortening occurred after, rather than before, A2 (25 (12) v -10 (2.5)% and 50 (30) v -6.6 (0.3)% total excursion, P < 0.001). Although the long axis lengthened a little at the start of early diastole, its dominant component occurred in late diastole to coincide with atrial systole. The relative A wave was thus greatly increased at both sites (67 (17) v 29 (6)% and 77 (13) v 33 (8)%, P < 0.001). CONCLUSION: Prolonged left ventricular long axis shortening and delayed onset of lengthening effectively suppress early diastolic transmitral flow even though the minor axis increases and mitral cusps separate apparently normally. This grossly asynchronous left ventricular relaxation may interfere with filling by dissipating normal ventricular restoring forces.

Aged↗

PubMed1995

Abnormal ventricular long-axis function in systemic sclerosis.

STUDY OBJECTIVE: To assess possible effects of systemic sclerosis on ventricular function. DESIGN: Retrospective analysis of patients referred for echocardiographic examination to assess ventricular function. SETTING: Tertiary referral center for cardiac and chest diseases equipped with invasive and noninvasive facilities. PATIENTS: Thirty-four patients with clinical diagnosis of systemic sclerosis, aged 49 +/- 12 years; 24 had pulmonary fibrosis and 10 did not. There were 21 normal controls of similar age. MEASUREMENTS: Two-dimensional guided M-mode echocardiographic recordings of the left ventricular minor and long axis at the left and septal sites and right ventricle were obtained. Transmitral and transtricuspid Doppler flow velocities were also obtained with ECG and phonocardiogram. RESULTS: In 24 patients with pulmonary fibrosis, long-axis excursion was reduced 2.1 +/- 0.5 vs 2.7 +/- 0.4 cm/s as was peak rate of shortening and lengthening, 8.5 +/- 3.3 vs 10.8 +/- 2.4 cm/s and 7.5 +/- 2.5 vs 12 +/- 3.6 cm/s, respectively (p < 0.001), at the right side compared with 10 patients without. The onset of right long-axis shortening and lengthening was delayed with respect to the Q wave of the ECG and P2 of the phonocardiogram (p < 0.001 in both vs controls). The onset of tricuspid forward flow from the second heart sound was also delayed in the two groups, 110 +/- 15 ms and 100 +/- 20 ms vs 80 +/- 15 ms, respectively (p < 0.001). Right ventricular late diastolic filling velocities were increased 35 +/- 15 and 35 +/- 12 cm/s vs 20 +/- 10 cm/s in both groups (p < 0.01), and hence E:A ratio reduced 1.25 +/- 0.5 and 1.4 +/- 0.3 vs 1.9 +/- 0.4, respectively (p < 0.001). Pulmonary flow acceleration time was reduced only in patients with pulmonary fibrosis, 105 +/- 30 ms vs 125 +/- 30 ms (p < 0.001). At the left side, total long-axis excursion was reduced only in patients with pulmonary fibrosis (p < 0.01), while peak shortening and lengthening rates were reduced in both groups (p < 0.05). The onset of shortening from the Q wave and lengthening from the second heart sound were both delayed in the two groups with the latter greatly delayed in patients with pulmonary fibrosis (p < 0.05). CONCLUSIONS: Right and left ventricular long-axis function is frequently abnormal in patients with systemic sclerosis. Abnormalities are more profound in patients with CT evidence of pulmonary fibrosis than in those without. We suggest that these disturbances are due to myocardial fibrosis which, from the anatomic distribution of longitudinally directed fibers, is likely to have been subendocardial.

Blood Flow Velocity↗

PubMed1994

Relations between resting ventricular long axis function, the electrocardiogram, and myocardial perfusion imaging in syndrome X.

OBJECTIVE: To investigate interrelations between ventricular long axis function, resting electrocardiogram, and myocardial perfusion imaging in a group of patients with syndrome X in order to define possible underlying mechanisms. DESIGN: Prospective echocardiographic, electrocardiographic, and myocardial perfusion imaging. SETTING: A tertiary referral centre for cardiac diseases with invasive and non-invasive facilities. PATIENTS: 50 consecutive patients with syndrome X selected on the basis of a history of angina, ST segment depression on exercise, and normal coronary arteriograms and 21 controls of similar age. RESULTS: Long axis motion of one or both ventricles assessed by echocardiography was abnormal in 37 patients. The onset of systolic shortening was delayed by > 130 ms (upper limit of normal 95% confidence interval) in eight patients, and was associated with prolonged shortening during the isovolumic relaxation period in seven (p < 0.01) (systolic abnormalities). The onset of diastolic lengthening was delayed by > 80 ms in 20. Early diastolic peak lengthening rate was < 4.5 cm.s-1 in 13 patients, and the relative amplitude of lengthening during atrial systole was > 45% in 18. On the resting electrocardiogram septal q waves were absent in 12 patients. This was associated with long axis systolic disturbances in seven patients (p < 0.05). T waves were abnormal in 10 and associated with delayed onset of early diastolic lengthening in all (p < 0.001). Late diastolic long axis disturbances were not associated with any consistent electrocardiographic abnormality. Myocardial perfusion imaging was abnormal in six of 33 patients, four of whom had systolic abnormalities (p < 0.03). Imaging was normal in the rest, but in 13 of them long axis function was abnormal in the left side and in four it was abnormal on the right ventricle. Both electrocardiography and imaging were normal in 10 patients. No patient with an abnormal electrocardiogram or myocardial perfusion had normal long axis motion on echocardiography. CONCLUSION: The function of the left and right ventricular long axes was abnormal in about 70% of a sample of patients with syndrome X. Systolic disturbances were consistently associated with absent septal q wave and abnormal myocardial perfusion imaging, while early diastolic disturbances correlated with T wave abnormalities. These associations suggest that the three different investigations detect related objective abnormalities in one or more subgroups of patients with syndrome X.

Echocardiography↗

PubMed1994

Abnormal subendocardial function in restrictive left ventricular disease.

OBJECTIVE: To study possible disturbances in left ventricular long axis function in patients with a restrictive filling pattern. DESIGN: Prospective examination of the left ventricular transverse and longitudinal axes, transmitral flow, and the apexcardiogram. SETTING: A tertiary referral centre for cardiac diseases. SUBJECTS: 21 normal subjects, age (SD) 51(11); 30 patients of similar age with a restrictive left ventricular filling pattern, defined as short early diastolic deceleration time less than the lower 95% confidence limit of the normal value (120 ms). 20 patients had a normal and 10 had an increased left ventricular end diastolic cavity size. RESULTS: Mitral Doppler echocardiography: E wave velocity was high only in patients with a normal cavity size. A wave velocity was greatly reduced in the two groups (P < 0.001) so that the E/A ratio was abnormally high. The relative A wave amplitude on the apexcardiogram was greatly increased in the two groups: 46(15)% (mean (SD)) and 54(4)% v 15(5)%. Minor axis: Fractional shortening was reduced from 30(10)% to 17(7)% in patients with normal cavity size and to 13(4.2)% in those with a dilated cavity (P < 0.001), as was the posterior wall thickening fraction from 100(30)% to 42(20)% and 50(25)% respectively (P < 0.001). Total systolic epicardial motion was normal and isovolumic relaxation time was short in the two groups. Long axis: Left ventricular abnormalities included reduced total amplitude of motion and its component during atrial systole (P < 0.001 for the two groups at both sites). Peak long axis shortening and lengthening were decreased at both left ventricular sites (P < 0.001). The time intervals from q wave of the electrocardiogram and A2 (aortic valve closure) to the onset of shortening and lengthening respectively were increased (both P < 0.001). Right ventricular long axis function was similarly affected but to a lesser extent. CONCLUSION: Left ventricular long axis function is consistently abnormal in patients with restrictive disease whether or not cavity size is increased. Not only are the extent and peak velocity of shortening reduced, but during diastole the peak early diastolic lengthening rate and amplitude during atrial systole are impaired. Early diastolic long axis motion is asynchronous with respect to transmitral flow and left ventricular minor axis. These effects will impair the overall left ventricular systolic and diastolic function independently of any decrease in passive cavity compliance. Unlike fibrosis, these long axis abnormalities are potentially amenable to treatment.

Cardiomyopathy, Restrictive↗

PubMed1993

Berheim "a" wave: obstructed right ventricular inflow or atrial cross talk?

OBJECTIVE: To study the possible mechanisms underlying the dominant "a" wave in the jugular venous pulse seen in patients with left ventricular hypertrophy (Bernheim "a" wave). DESIGN: Prospective examination of the left ventricular transverse and longitudinal axes, transmitral and transtricuspid flows, and jugular venous pulse recordings. SETTING: Tertiary referral centre for cardiac disease. SUBJECTS: 23 patients with left ventricular hypertrophy of various aetiologies and a dominant "a" wave in the jugular venous pulse. Controls were 21 normal volunteers. RESULTS: Early diastolic filling of the right ventricle was normal. During right atrial systole the (mean(SD)) tricuspid ring motion was exaggerated (1.2(0.4) v 0.8(0.2) cm, p < 0.001) and Doppler A wave velocity slightly increased (0.3(0.1) v 0.2(0.08) m/s, p < 0.01), although the E wave remained dominant. By contrast left ventricular isovolumic relaxation time was longer than normal (70(20) v 55(10) ms, p < 0.001) with wall motion incoordinate in the septal long axis, 15%(9.5%) v 6.6%(3%) total excursion occurring before mitral valve opening. During early filling the extent of long axis motion was decreased to 0.6(0.5) cm from 1.1(0.2) cm, (p < 0.001) and 0.5(0.2) cm from 0.9(0.2) cm, (p < 0.0001) at the left and septal sites, and similarly its peak lengthening rate reduced to 5.4(2.5) cm/s from 10(3) cm, (p < 0.001) and 4.3(2.2) cm/s from 8(2) cm, (p < 0.001). The atrial component of long axis lengthening was increased to 43%(18%) from 29%(6%) (p < 0.01) and 55%(15%) from 33%(8%) of the total excursion (p < 0.0001). Left ventricular E/A ratio was less than normal (0.9(0.8) v 1.4(0.4), p < 0.05). CONCLUSIONS: There is no evidence of obstruction or any other disturbance of early diastolic right ventricular inflow in Bernheim's syndrome. It is possible that the haemodynamically appropriate increase in left atrial activity is mirrored on the right side due to shared interatrial myocardial fibres. This could represent a form of atrial interaction.

Adult↗

PubMed1993

Early changes in left ventricular subendocardial function after successful coronary angioplasty.

OBJECTIVE: To study the early effects of coronary angioplasty on resting left ventricular long axis function, reflecting that of the subendocardium. DESIGN: Prospective echocardiographic and Doppler examination of patients with coronary artery disease, before and after single vessel coronary angioplasty. SETTING: A tertiary referral centre for cardiac diseases with facilities for invasive and non-invasive investigation. PATIENTS: 23 patients with significant left coronary disease being considered for coronary angioplasty. RESULTS: Before angioplasty the mean (SD) isovolumic relaxation time was longer than normal (75(19) ms v 55 (10), p < 0.001) with a significant increase in transverse dimension change before mitral valve opening, and peak rate of early diastolic thinning (8(3) v 10.4 (2.6) cm/s (p < 0.001)) was reduced. Long axis motion was frequently abnormal. The interval from the onset of the Q wave to the onset of shortening was prolonged (118 (30) ms v 90 (19) at the left site and 115 (26) ms v 81 (9) at the septal site, p < 0.001) and the onset of early diastolic rapid lengthening delayed with respect to the aortic valve closure sound (A2) by 85 (34) ms v 58 (11) at the left site and 88 (33) ms v 60 (9) at the septal site (p < 0.001). Although overall amplitude was reduced at the septal site only (1.23 (0.3) cm v 1.5 (0.4), p < 0.05), the extent (0.8 (0.2) cm v 1.04 (0.3) at the left site and 0.66 (0.2) cm v 0.9 (0.3) at the septal site, p < 0.001) and peak rate (6.2 (2) cm/s v 10 (2.5) at the left site and 5.4 (2.3) cm/s v 8.5 (2) at the septal site, p < 001) of early diastolic lengthening were both much lower than normal. The E/A ratio on transmitral Doppler was modestly reduced (1.0 (0.7) v 1.4 (0.4), p < 0.05). After angioplasty: isovolumic relaxation time shortened to 64 (18) ms (p < 0.001) and left ventricular incoordination regressed. Long axis shortening with respect to Q (98 (32) ms v 118 (30) at the left site and 94 (23) ms v 115 (26) at the septal site, p < 0.01) and that of lengthening with respect to A2 both normalised. Early diastolic peak lengthening rate increased (7.5 (2.1) cm/s v 6.2 (2) at the left site, and 6.3 (2.4) cm/s v 5.4 (2.3) at the septal site, p < 0.001). The early diastolic peak thinning rate of the posterior wall significantly increased (10 (3.5) cm/s v 8 (3), p < 0.005) as did mitral E/A ratio 1.2 (0.7) v 1.0 (0.7), p < 0.05). CONCLUSION: Long axis motion, representing the function of longitudinally arranged subendocardial fibres, is consistently abnormal in the resting state in coronary artery disease. These systolic and diastolic abnormalities return towards normal after successful angioplasty, suggesting that they are the direct effect of coronary artery stenosis.

Angioplasty↗