Clinical significance of incomplete tricuspid valve closure seen on two-dimensional echocardiography.

Incomplete closure of the tricuspid valve without apparent cusp disease was noted on two-dimensional echocardiography in 31 patients. This abnormality was defined as a failure of the tricuspid valve leaflet tips to reach the plane of the tricuspid valve anulus by at least 1 cm in the standard apical four chamber view at the point of maximal systolic closure. This resulted in a final systolic leaflet position deeper within the right ventricular cavity than is normally seen. The finding was present in the following diagnostic subgroups: Group A, pulmonary hypertension (11 patients); Group B, rheumatic heart disease (4 patients); Group C, dilated cardiomyopathy (9 patients) and Group D, previous myocardial infarction (7 patients). Right atrial, right ventricular and tricuspid anulus measurements were made and compared with those from a group of 67 normal subjects. The results were as follows: right atrial endsystolic area = 27.2 +/- 8.6 cm2 (normal = 13.4 +/- 2.0); right ventricular end-systolic area = 25.6 +/- 8.7 cm2 (normal = 10.9 +/- 2.9); right ventricular end-diastolic area = 31.5 +/- 9.1 cm2 (normal = 20.1 +/- 4.9) and tricuspid valve anular end-systolic dimension = 4.0 +/- 0.6 cm (normal = 2.2 +/- 0.3). The differences from the normal data were all statistically significant (p less than 0.001). Incomplete closure of the tricuspid valve, although a nonspecific diagnostic finding, is primarily associated with right-sided chamber enlargement. Tricuspid regurgitation may be present. The mechanism could be related to geometric changes in valve apparatus dynamics secondary to right-sided cardiac enlargement and tricuspid valve anular dilation.(ABSTRACT TRUNCATED AT 250 WORDS)

The natural history of left ventricular thrombus in myocardial infarction: a rationale in support of masterly inactivity.

One hundred five unselected and consecutive patients were prospectively studies after acute transmural myocardial infarction to assess the incidence of mural thrombus formation and to relate the presence of thrombus to patient outcome in terms of systemic embolic events, functional class and survival. In 87 patients, optimal quality two-dimensional echocardiographic studies were obtained and were repeated at daily intervals to detect mural thrombus formation. The site of infarction was anterior in 53 patients and inferior in 34. On admission, all patients received subcutaneous heparin and antiplatelet agents (aspirin, dipyridamole); none received full anticoagulant therapy. Left ventricular mural thrombus was visualized between 2 and 11 days (median 6) after the clinical onset of infarction in 21 (40%) of the 53 patients with anterior infarction. No patients with inferior infarction had echocardiographic evidence of thrombus formation. During follow-up of 22 to 51 months (mean 39), none of the 21 patients with mural thrombus had clinical evidence of systemic embolism. One patient with inferior and one with anterior infarction had a cerebral embolus 7 days and 9 months, respectively, after the acute event, but neither of these patients had echocardiographic evidence of left ventricular thrombus at any stage. Echocardiography performed at 1 and 2 years of follow-up showed persistent evidence of thrombus in only 8 (31%) and 5 (24%) of the 21 patients, respectively. On admission, the functional class of patients with anterior myocardial infarction and thrombus was similar to that of patients without ventricular thrombus.(ABSTRACT TRUNCATED AT 250 WORDS)

Pseudoaneurysm of the pulmonary artery after the banding procedure: two-dimensional echocardiographic description.

This report describes an infant with double-outlet right ventricle who underwent pulmonary artery banding as palliation for excessive left to right shunting through a ventricular septal defect. Three weeks after this procedure, there was abrupt clinical deterioration, and two-dimensional echocardiography clearly defined a large pseudoaneurysm arising from a breach in the posterior pulmonary artery wall, just proximal to the band. The diagnosis was confirmed at surgery, during which total correction was performed with successful outcome. The two-dimensional echocardiographic features of a pseudoaneurysm of the pulmonary artery are shown and the role of this noninvasive technique in the evaluation of pulmonary artery bands is discussed.

Comparison of the echocardiographic and hemodynamic diagnosis of rheumatic tricuspid stenosis.

Two-dimensional echocardiography has proved to be reliable in the diagnosis of mitral, aortic and pulmonary stenosis. Its role in the diagnosis of rheumatic tricuspid stenosis is still being defined; therefore, the tricuspid valve echograms of 147 patients with rheumatic heart disease were examined. Thirty-eight of these patients also underwent hemodynamic evaluation. Tricuspid stenosis was defined echocardiographically as diastolic anterior leaflet doming, thickening and restricted excursion of the other two tricuspid leaflets and decreased separation of the leaflet tips. Using these criteria, the sensitivity and specificity of the echocardiogram in detecting tricuspid stenosis were 69 and 96%, respectively, in the group of 38 patients who had both echocardiographic and hemodynamic evaluations. However, when the smaller group of 17 patients who had simultaneous right atrial and right ventricular pressure recordings were considered separately, there was complete agreement between the echocardiographic and hemodynamic data. Thus, the two-dimensional echocardiogram is a sensitive and specific test for diagnosing rheumatic tricuspid stenosis. In addition, these data provided an opportunity to determine the prevalence of tricuspid stenosis in this group of patients with chronic rheumatic valvular disease. Tricuspid stenosis was present in 14 (9.5%) of the total group of 147 patients who had two-dimensional echocardiograms, and in 10 (26.3%) of the 38 who had both echocardiographic and hemodynamic studies. In patients with rheumatic heart disease about to undergo cardiac catheterization, an echocardiographic study should prove useful in making the diagnosis of tricuspid stenosis.

The natural history of regional wall motion in the acutely infarcted canine ventricle.

Two-dimensional echocardiography was employed to define the natural history of regional wall motion abnormalities in a canine model of acute experimental myocardial infarction. Serial short-axis two-dimensional echocardiograms were recorded in 11 closed chest dogs before coronary occlusion and 10, 30, 60, 180 and 360 minutes after permanent coronary ligation. Radiolabeled microsphere-derived blood flows were obtained in each study period and the histochemical (triphenyltetrazolium chloride) extent of infarction was determined at 6 hours. Previously published methods were used to quantitate field by field (every 16.7 ms) excursion of 36 evenly spaced endocardial targets. The circumferential extent of abnormal wall motion was followed sequentially using previously published definitions of abnormality: 1) systolic fractional radial change of less than 20%; 2) dyskinesia (systolic bulging) at the point in time (echocardiographic field) in which there is maximal dyskinesia; and 3) correlation with composite normal ray motion falling outside the 95% confidence limits defined in the control period. On the basis of the triphenyltetrazolium chloride staining pattern, the ventricle was divided into five zones: central infarct zone, zone with greater than 25% transmural infarction, total infarct zone, border zones and normal zone. Mean systolic fractional radial change was calculated for each zone and used as an index of the magnitude of abnormal wall motion. Regardless of the definition of abnormality employed, the circumferential extent of abnormal wall motion manifested at 10 minutes after occlusion did not significantly change, even up to 6 hours later. Similarly, 10 minutes after coronary occlusion the three infarct zones and border zones demonstrated significantly reduced systolic fractional radial change. This remained stable over the remainder of the 6 hour study period. It is concluded that once established at 10 minutes after coronary occlusion, the circumferential extent and magnitude of abnormal wall motion do not significantly change in the immediate postinfarct (6 hour) period.

An echocardiographic technique for quantifying and displaying the extent of regional left ventricular dyssynergy.

A convenient noninvasive method of mapping the left ventricular endocardial surface has been developed that can be used to display regional dysfunction and calculate the total area of abnormal endocardial excursion from data obtained in two orthogonal apical and three or more short-axis cross-sectional echocardiographic images. Visually identified regions of abnormal systolic function are plotted on end-diastolic, planar endocardial surface maps, and the extent of dysfunction can be expressed either as an absolute area or as a fraction of the total endocardial surface area involved. The extent of the left ventricular surface moving abnormally, calculated with this echocardiographic mapping technique, was compared with two histochemical measures of infarct size in a series of 11 closed chest dogs with acute circumflex coronary artery occlusions. Overall extent of abnormally moving left ventricular wall correlated closely with both the fraction of the endocardial area overlying infarct (r = 0.92, p less than or equal to 0.001) and the fraction of the myocardial volume infarcted (r = 0.86, p less than or equal to 0.001). This suggests that the echocardiographic mapping technique can be used to accurately quantify the global extent of abnormal systolic function in the presence of regional wall motion abnormalities.

The effects of antihypertensive therapy on carotid vascular structure in man.

OBJECTIVE: An increased carotid intima-media thickness (IMT) has been found to be associated with a number of cardiovascular risk factors such as age, hypertension, cigarette smoking, hypercholesterolaemia and left ventricular hypertrophy. Our objective was to assess whether carotid intima-media thickness in hypertensive patients could be reduced by antihypertensive therapy. METHODS: 13 hypertensive patients, 10 previously untreated, were examined using carotid ultrasonography and echocardiography at baseline and then at 8 weeks and 39 weeks after commencement of antihypertensive therapy with ramipril and the second-line addition of felodipine. RESULTS: By the end of the study significant regression of IMT (0.1(0.05-0.16) mm, F-value 10.2, P < 0.01) and left ventricular mass index had occurred (25(10.7-39.3) g/m2, F-value 9.7, P < 0.01). The reduction in IMT was significantly related to the reduction in mean arterial pressure, r = 0.55, P = 0.05). CONCLUSION: Antihypertensive therapy with ramipril and felodipine causes regression of IMT in hypertensive patients, probably chiefly through blood pressure reduction. Large prospective studies are required to assess whether a reduction in IMT results in a reduction in morbidity and mortality.

Left ventricular hypertrophy and QT dispersion in hypertension.

The interlead variation in QT length on a standard electrocardiograph reflects regional repolarization differences in the heart. To investigate the association between this interlead variation (QT dispersion) and left ventricular hypertrophy, we subjected 100 untreated subjects to 12-lead electrocardiography and echocardiography. Additionally, 24 previously untreated subjects underwent a 6-month treatment study with ramipril and felodipine. In the cross-sectional part of the study, QT dispersion corrected for heart rate (QTc dispersion) was significantly correlated with left ventricular mass index (r = .30, P < .01), systolic pressure (r = .30, P < .01), the ratio of peak flow velocity of the early filling wave to peak flow velocity of the atrial wave (E/A ratio) (r = -.22, P = .02), isovolumic relaxation time (r = .31, P < .01), and age (r = .21, P < .04). In the treatment part of the study, lead-adjusted QTc dispersion decreased from 24 to 19 milliseconds after treatment, and after a subsequent 2 weeks of drug washout remained at 19 milliseconds (P < .01). The changes in left ventricular mass index at these stages were 144, 121, and 124 g/m2 (P < .01). Systolic pressure decreased from 175 to 144 mm Hg and increased again to 164 mm Hg after drug washout (P < .01). The E/A ratio (0.97, 1.02, and 1.02; P = 69) and isovolumic relaxation time (111, 112, and 112; P = .97) remained unchanged through the three assessment points. In conclusion, QT dispersion is increased in association with an increased left ventricular mass index in hypertensive individuals. Antihypertensive therapy with ramipril and felodipine reduced both parameters. If an increased QT dispersion is a predictor of sudden death in this group of individuals, then the importance of its reduction is evident.

Ethnic differences in the hypertensive heart and 24-hour blood pressure profile.

Black hypertensive persons have been observed to have a greater degree of left ventricular hypertrophy than white hypertensives. However, previous studies have matched groups for blood pressure (BP) measured in the clinic, and it has been demonstrated that black hypertensives have an attenuated nocturnal BP dip. Clinic BPs may thus underestimate mean 24-hour BP in this group. To investigate whether the differences in left ventricular hypertrophy can be accounted for by the greater mean 24-hour BP in black hypertensives, 92 previously untreated hypertensives were studied with 24-hour ambulatory BP monitoring and echocardiography. The 46 black hypertensives (24 men and 22 women) were matched with the 46 white hypertensives for age, gender, and mean 24-hour BP. Despite similar mean 24-hour BPs (blacks, 142/93 mm Hg; whites, 145/92 mm Hg; P=.53/.66), the black group had a smaller mean nocturnal dip than the white group (blacks, 8/8 mm Hg; whites, 16/13 mm Hg; P<.01). In addition, mean left ventricular mass index (LVMI) was greater (blacks, 130 g/m2; whites, 107 g/m2; P<.001). Mean 24-hour systolic BP was significantly related to LVMI in both groups (blacks, r=.45, P<.01; whites, r=.56, P<.01). However, systolic BP dip correlated inversely with LVMI only in the black group (blacks, r=-.30, P<.04; whites, r=.05, P=.76). In a multiple regression model, LVMI was independently related to both mean daytime BP and mean nocturnal BP dip in black subjects but only to mean daytime BP in white subjects. In conclusion, the increased left ventricular hypertrophy observed in black hypertensives compared with white hypertensives is not accounted for by differences in mean 24-hour BP. However, LVMI in black hypertensives appears to be more dependent on nocturnal BP than that in white hypertensives; this, coupled with the attenuated BP dip in black hypertensives, suggests that the BP profile rather than 24-hour BP may be important in determining the differences in left ventricular hypertrophy.

Ventricular arrhythmias in hypertension: in which patients do they occur?

OBJECTIVE: It has been suggested that the increased incidence of sudden death in hypertensive patients, particularly those with left ventricular hypertrophy, may be casually related to the increased number and complexity of ventricular arrhythmias that have been demonstrated in these patients. The objective of the present study was to assess some of the factors which might be responsible for these arrhythmias. SUBJECTS AND METHODS: One hundred and three untreated subjects were divided into four groups on the basis of blood pressure and echocardiographic measurements: hypertensive patients with left ventricular hypertrophy (n = 38), hypertensive patients without left ventricular hypertrophy (n = 16), patients with borderline or white-coat hypertension (n = 26) and normotensive subjects (n = 23). Each subject underwent two-dimensional and Doppler echocardiography, 12-lead electrocardiogram examination, 12-lead electrocardiogram exercise stress testing, 24-h ambulatory blood pressure monitoring and 24-h Holter monitoring. A further 17 hypertensive patients with left ventricular hypertrophy who were on long-term antihypertensive therapy were also investigated in the same manner and compared with untreated hypertensive patients with left ventricular hypertrophy who were matched for age, sex and race. RESULTS: Untreated hypertensive patients, even with left ventricular hypertrophy, had a low prevalence of frequent or complex arrhythmias (seven out of 80 patients with Lown score 2+). In contrast, hypertensive patients with left ventricular hypertrophy on long-term antihypertensive therapy had a significantly greater prevalence of complex arrhythmias than untreated patients with left ventricular hypertrophy (eight out of 17 treated patients compared with two out of 17 untreated patients with Lown score 2+). CONCLUSIONS: Hypertensive patients with left ventricular hypertrophy who had received long-term antihypertensive therapy were found to have a high prevalence of complex ventricular arrhythmias, which was in contrast to untreated hypertensive patients, even those with left ventricular hypertrophy. This may reflect the consequences on the left ventricle of long-term antihypertensive treatment. If complex ventricular arrhythmias are implicated in the excess of sudden deaths in hypertensive patients, this might be an important factor.

Comparison of exercise echocardiography with an exercise score to diagnose coronary artery disease in women.

This study compares the accuracy of the routine exercise electrocardiogram, exercise score, and exercise echocardiography for the diagnosis of coronary artery disease (CAD) in women. Seventy women with a pretest probability of 53 +/- 30% for CAD were stressed using a maximal symptom-limited bicycle exercise protocol. Significant ST-segment change was defined by a depression of > 0.1 mV 0.06 second after the J point. The exercise score was calculated from ST response, heart rate, and workload using an equation derived from a multivariate model. A positive stress echocardiogram was defined by development of a new or worsening wall motion abnormality. The results were compared with the presence or absence of significant (> 50% diameter) stenoses at angiography. Exercise echocardiography identified 29 of the 33 patients (88%) with CAD, compared with 22 (67%) using ST analysis alone, and 20 (61%) using the exercise score (both p < 0.05 vs exercise echocardiography). The specificity of exercise echocardiography (84%) and the multivariate score (73%) were comparable, and exceeded that of the ST analysis (51%) in 37 patients without CAD (p < 0.01). The accuracy of exercise echocardiography (86%) exceeded that of the exercise score (67%, p = 0.01) and ST analysis (59%, p < 0.01). Among all 70 patients, an intermediate (20% to 80%) probability of coronary disease was identified in 21 patients on the basis of exercise echocardiography, in 38 based on the multivariate score, and in 38 based on the ST analysis alone. Exercise echocardiography is more sensitive than the exercise score, and more sensitive and specific than ST-segment analysis for the diagnosis of CAD in women.(ABSTRACT TRUNCATED AT 250 WORDS)

Limitations of dipyridamole-echocardiography in effort angina pectoris.

The sensitivity of dipyridamole--2-dimensional (2-D) echocardiography was assessed for detection and localization of ischemia in 21 patients with severe chronic stable angina pectoris, a clearly positive exercise stress test response and multivessel coronary atherosclerosis. Regional wall motion during dipyridamole infusion (0.6 mg/kg intravenously over 4 minutes) was compared with control and recovery by 2 blinded observers in consensus. Transient regional wall motion abnormalities were observed in 11 patients. Angina and ST-segment changes occurred in 9 of these 11 patients with positive responses, but in none of those who showed no transient abnormality of regional wall motion. Localization of regional wall motion abnormalities correlated well with angiographic severity of coronary lesions. Endocardial area contraction, evaluated by a computerized system, was reduced significantly after dipyridamole administration in patients with a positive response (from 51 +/- 10% to 35 +/- 11%, p less than 0.001), whereas it did not change significantly in the others (from 43 +/- 6% to 42 +/- 8%). In the 11 patients with a positive response, coronary reserve assessed by exercise testing (modified Bruce protocol) was more impaired than in those with a negative response (time to 1 mm of ST depression 177 +/- 148 seconds and 472 +/- 179 seconds, respectively, p less than 0.01). In patients with severe angina and multivessel coronary artery disease, dipyridamole--2-D echocardiography appears to identify the vessel in which flow reserve is most limited. Although this information may be valuable, indications for the test are restricted to patients with severely limited exercise capacity.

Relation between coronary artery disease, baseline clinical variables, revascularization mode, and mortality. CABRI Participants. Coronary Angioplasty vs. Bypass Revascularisation Investigation.

The Coronary Angioplasty vs. Bypass Revascularisation Investigation (CABRI) trial comparing percutaneous transluminal coronary angioplasty (PTCA) with coronary artery bypass grafting did not show a difference in mortality with either procedure. Nonrandomized studies suggest that coronary artery disease (CAD) severity and distribution influences outcome. In the present study we explored the effect of prerevascularization CAD on 1-year mortality in the CABRI population, while adjusting for other baseline variables. Of the 1,054 patients recruited, there were sufficient angiographic results to derive the CAD scores in 974 (92.4%). Of these 974, there were 32 deaths. A number of CAD scores, both weighted for proximal disease (Duke and Leaman) and nonweighted, were used. These scores were then cross-tabulated against mortality. Demographic and clinical variables were also cross-tabulated against mortality and used to derive an initial logistic regression model to predict mortality. The effect of adding each of the CAD scores to this initial model was then assessed. After inclusion of the CAD scores, the best model was: (1) presence of peripheral vascular disease (odds ratio [OR] 3.89, p = 0.0025), (2) previous cerebrovascular accident (OR 2.86, p = 0.043), (3) older age (OR 1.05, p = 0.039), (4) a higher Duke score (OR 2.84, p = 0.0061), and (5) having undergone PTCA (OR 2.12, p = 0.047). In the CABRI population, adjustment for baseline variables, including prerevascularization CAD, revealed significantly higher mortality in those who underwent PTCA than in those who underwent coronary artery bypass grafting.

Atenolol with and without nifedipine in the treatment of angina pectoris. Preliminary report.

Atenolol and nifedipine have been shown to be effective single agents in angina pectoris, but reports suggest that additional benefits may be conferred by combining the 2 drugs. Therefore, to establish that the combination regimen was at least as effective as either atenolol or nifedipine alone, a multicentre study was performed to compare the treatment regimens in 94 patients with characteristic chest pain compatible with a diagnosis of stable angina pectoris which was provoked by effort and relieved by glyceryl trinitrate. After 4 weeks on atenolol 50 mg twice daily, the patients were randomised to receive, in a double-blind crossover fashion, atenolol 50 mg twice daily either with or without sustained release nifedipine 20 mg twice daily for 4 weeks. Compared with entry, all treatments apparently reduced the number of anginal attacks per week and the number of glyceryl trinitrate tablets taken. It was notable that blood pressure in patients during the study was normal. Treatment with atenolol or the combination appeared to improve exercise tests measured by time to onset of pain, time to greater than or equal to 1mm ST segment depression and duration. The ST segment depression was substantially lower on the fixed combination compared with atenolol alone; ST segment depression during exercise was recorded in 82% of patients after atenolol and 75% after the combination, compared with 100% on entry. There was a substantial improvement in the number of patients rendered pain free: 29% on atenolol and 42% on combination. There was little difference between treatments in terms of adverse effects.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects on cardiac arrhythmias of antihypertensive therapy causing regression of left ventricular hypertrophy.

To examine the effects of antihypertensive therapy causing regression of left ventricular hypertrophy on cardiac arrhythmias, 26 hypertensive subjects were treated with ramipril with felodipine if required, and followed for 6 months after blood pressure control. Compared with baseline, left ventricular mass index (LVMI) was significantly reduced both at blood pressure control and after a further 6 months of treatment (baseline, blood pressure control, 6 months after blood pressure control; LVMI 142 +/- 3.6, 131 +/- 3.4, 123 +/- 3.8* g/m2, *P < .01 compared with baseline). There was a significant relationship between the decrease in systolic blood pressure and the decrease in LVMI after 6 months of blood pressure control compared with baseline (r = 0.41, P = .05). Compared with baseline, the average total number of ventricular ectopics decreased after blood pressure was controlled (88 +/- 59 and 21 +/- 12 respectively); however this reduction was not maintained after 6 months of further treatment, either before (78 +/- 50) or after drug washout (86 +/- 40). Compared with baseline (639 +/- 590) supraventricular ectopic total was not initially reduced after blood pressure control (650 +/- 604), but was reduced after a further 6 months of treatment (294 +/- 261). This reduction was maintained after drug washout (267 +/- 254), although this did not reach statistical significance. Radionuclide scanning at baseline was not a predictor of patients with the highest risk of arrhythmia and there was no correlation between improvement or worsening of a defect with changes in ventricular ectopic total. In conclusion, antihypertensive therapy with ramipril and felodipine, although causing regression of left ventricular hypertrophy did not lead to a sustained reduction in ventricular ectopic total.

Ethnic differences in the identification of left ventricular hypertrophy in the hypertensive patient.

Left ventricular hypertrophy (LVH) is more prevalent in black than white hypertensives, but this difference is greater when identified by electrocardiography (ECG) than by echocardiography. We evaluated the proposal that current ECG criteria for LVH are less specific, and therefore, less useful, in blacks than whites. In a retrospective cross-sectional study, 408 subjects (271 white, 137 black) referred to a hypertension clinic for assessment of hypertension underwent measurement of blood pressure, ECG voltages (Sokolow-Lyon and Cornell sex-specific), and echocardiographic left ventricular mass index (LVMI). Black subjects had greater ECG voltages than whites, even when closely matched for LVMI. In black subjects, current ECG criteria were twice as sensitive as in whites (Sokolow-Lyon: 44.9% v 22.5%, P = .003. Cornell: 30.4% v 15.7%, P = .03). They were less specific in blacks using the Sokolow-Lyon criteria (73.5% v 86.8%, P = .02) but this failed to reach significance using the Cornell criteria (83.8% v 91.8%, P = .07). When voltage criteria were adjusted to give matched sensitivities and specificities, respectively, differences in specificity and sensitivity were no longer apparent. Receiver operating characteristic curve analyses confirmed no significant differences in overall performance of either ECG criteria between blacks and whites. In conclusion, ECG detection of LVH is insensitive in both ethnic groups. Sensitivity is higher in blacks due to higher LVMI in those with LVH. Apparent differences in specificity are due to ethnic differences in ECG voltages that are unrelated to differences in LVMI. When these differences are taken into account, there are no overall differences in test accuracy. However, given the prognostic importance of the detection of LVH, currently accepted ECG voltage criteria for the detection of LVH remain of equal or greater value in black hypertensives compared with whites.

Minimally invasive coronary revascularization through parasternal incisions without cardiopulmonary bypass.

BACKGROUND: We report the results of minimally invasive coronary revascularization without cardiopulmonary bypass through miniparasternal incisions. METHODS: This procedure was performed in 40 patients with disease in the left anterior descending, first diagonal, and right coronary arteries. After a 5- to 7-cm left vertical parasternal incision and removal of two costal cartilages, the left internal mammary artery was harvested up to the 2nd rib. The left anterior descending artery was occluded by means of two polydioxanone monofilament sutures. The anastomosis was performed with one 7-0 Prolene suture while the heart was beating. In 4 cases the left internal mammary artery was used as a sequential graft to the left anterior descending artery and the first diagonal artery. In 14 cases the right coronary artery was grafted with the right internal mammary artery through a right parasternal incision. Postoperatively, 95% of the patients underwent angiographic assessment of the anastomoses. RESULTS: We performed 52 anastomoses (34 to the left anterior descending artery, 4 to the first diagonal artery, and 14 to the right coronary artery). The mortality was 0% and the morbidity included postoperative bleeding (5%), acute renal failure (2.5%), atrial fibrillation (2.5%), and wound infection (5%). No patient had ventricular arrhythmias or circulatory problems during or after the operation. Two patients (5%) with right internal mammary artery-to-right coronary artery grafting had graft failure that required a redo operation. CONCLUSIONS: Small vertical parasternal incisions may be an alternative approach for single and multiple coronary revascularization, with a low incidence of intraoperative cardiac complications. The application of this approach to the right coronary artery, however, carries additional technical difficulties, and careful patient selection may be required to achieve optimal results.

Stress echocardiography for the diagnosis of ischaemia in hypertensives.

Exercise treadmill electrocardiography and myocardial perfusion imaging are commonly used in non-invasive tests for the detection of myocardial ischaemia. Unfortunately there are limitations in the assessment of hypertensive patients since these tests frequently provide false-positive results, particularly in those subjects with left ventricular hypertrophy. In order to investigate the utility of stress echocardiography in hypertensive patients we assessed 173 subjects undergoing this investigation in our department. Of these, 66 had had coronary angiography within 6 months. Thirty subjects were hypertensives, 17 with left ventricular hypertrophy, and 36 normotensives. Patients with a 70% or greater stenosis at coronary angiography were deemed to have sufficient disease to cause myocardial ischaemia. The overall sensitivity of stress echocardiography for detecting myocardial ischaemia was 83% with a specificity of 77%. For the hypertensive group alone the sensitivity was 93% and specificity 73%. The normotensives had a sensitivity of 76% with a specificity of 80%. In conclusion, in this group of hypertensives stress echocardiography had a favourable specificity and this was not significantly different from that of normotensive subjects. Journal of Human Hypertension (2000) 14, 399-401

Intraventricular dispersion of E wave velocity: an alternative measure of left ventricular diastolic function in hypertensive patients?

The E/A ratio (of peak mitral blood flow velocity during early diastole to that during atrial contraction) has limitations in the assessment of diastolic function. Previous studies have suggested that peak blood flow velocity is normally maintained or increased towards the cardiac apex but that it decreases in diastolic dysfunction. We evaluated the proposal that intraventricular dispersion of E wave velocity is an effective means of assessing diastolic function in hypertensives. Fifty-five untreated hypertensive patients underwent echocardiographic examination. Pulsed-wave Doppler recordings were made from the apical four-chamber view. Peak flow velocities were measured during early diastole at the level of the mitral valve (E0), and 3 cm distally (E3), and during atrial contraction at the level of the mitral valve (A). Mean peak flow velocities were 64.4 +/- 16.1 m/s for E0, 50.6 +/- 17.9 m/s for E3 and 61.1 +/- 12.1 m/s for A. Peak flow velocity during early diastole slowed towards the cardiac apex in most patients (E3/E0 range: 0.42-1.86, mean 0.81 +/- 0.29). There was no significant difference in E3/E0 between those with and without left ventricular hypertrophy (LVH) (0.76 +/- 0.25 vs 0.82 +/- 0.29, P = 0. 39). E3/E0 did not correlate with age (r = -0.02, P = 0.89), systolic blood pressure (BP) (r = 0.17, P = 0.20), diastolic BP (r = 0.21, P = 0.12) or LVMI (r = -0.11, P = 0.40). In contrast the E/A ratio correlated strongly with age (r = -0.66, P < 0.0001) and negatively, though not significantly, with systolic BP (r = -0.24, P = 0.07), diastolic BP (r = -0.23, P = 0.09) and LVMI (r = -0.23, P = 0.08). Although there is some intraventricular dispersion of E wave velocity in this group of hypertensive patients, the ratio of E3/E0 correlates poorly with parameters which are known to influence diastolic function. In spite of its limitations, the E/A ratio appears to be a more reliable measure of diastolic function in hypertensive heart disease than intraventricular dispersion of early diastolic filling.

Left ventricular geometry in presenting untreated hypertension.

In order to investigate the spectrum of geometry in our patient population, 63 untreated hypertensives underwent two-dimensional echocardiography. Left ventricular (LV) mass index and relative wall thickness, a measure of wall thickness in relation to cavity size, were calculated from the M-mode strip. In addition, to assess the sphericity of the left ventricle the ratio of LV minor to major hemiaxis was calculated. The subjects comprised 41 men (17 Caucasian, 22 Afro-Caribbean and two Oriental), and 21 women (five Caucasian, 12 Afro-Caribbean and two Oriental). Concentric hypertrophy was present in 46% of subjects, concentric remodelling in 32% of subjects, eccentric hypertrophy in only 6% of subjects and a normal left ventricular shape in 16% of subjects. The degree of sphericity of the left ventricle was similar among the four groups, suggesting that it does not change in uncomplicated hypertension. In contrast to the previously published combined series from Sassari and New York we had a low proportion of patients with either eccentric hypertrophy or normal left ventricular geometry. This is probably due to the high proportion of Afro-Caribbean subjects in our clinic population who are more likely to have left ventricular hypertrophy.