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Clinical and electrophysiological characteristics have been investigated in a group of 30 patients with a sick sinus syndrome. No predictable response to exercise or drugs was observed, although a poor response of the sinus rate to atropine was present. Distal conduction abnormalities were found in seven of 14 patients, in whom detailed electrophysiological measurements were made, and sinus node recovery time was abnormal in all except one. Treatment with permanent pacing not only relieved syncope and dizziness, but made drug treatment of associated tachyarrhythmias feasible. The elusive and intermittent nature of the syndrome is stressed. The pathological findings in one case are described at length.

Objectives. This study sought to identify risk factors for both late observed and late “excess” mortality after aortic valve replacement and to examine the causes of late mortality. Background. Because operative mortality after aortic valve replacement is very low, the timing of surgical intervention should focus on maximizing long-term survival. However, to judge the effect of valve replacement on long-term survival in an elderly population, it is important to separate mortality resulting from extraneous causes ( background mortality ) from disease-related mortality ( excess mortality ). Background mortality can be estimated by calculating expected mortality on the basis of age and gender. Methods. From 1966 to 1986, 643 patients (mean age 59.6 years, 138 [21%] ≥70 years old) underwent aortic valve replacement, 129 of whom also underwent coronary bypass grafting; 594 patients survived ≥30 days after the procedure. The overall operative mortality rate for isolated aortic valve replacement decreased over time from 25.5% (1966 to 1972) to 2.6% (1980 to 1986). Cumulative total follow-up after discharge was 3,603 patient-years. Multivariate analysis was performed for both observed and excess mortality. Results. Risk factors for both observed and excess mortality were previous myocardial infarction, coronary artery disease, heart failure and atrial fibrillation. Although age ≥70 years was a risk factor for observed mortality (hazard rate ratio [HRR]2.4, 95% confidence interval [CI] 1.6 to 3.7), it was not a risk factor for excess mortality. In contrast, isolated aortic regurgitation was an important risk factor for excess mortality only (HRR 3.8, 95% CI 1.3 to 11.2). Late mortality was valve related in 22% of patients, including sudden death in 7% and cerebral vascular accidents in 7%. Congestive heart failure was an important cause of death (21%) irrespective of the time elapsed since aortic valve replacement. In patients with aortic regurgitation, congestive heart failure was the main cause of death (38%); in patients with aortic regurgitation and preoperative heart failure or severe left ventricular dysfunction, heart failure was the cause of death in 44% and 63%, respectively. Conclusions. Analysis of excess mortality revealed that older age in itself is not a risk factor for late mortality after aortic valve replacement. Aortic regurgitation carries a high risk, probably associated with left ventricular dysfunction at the time of operation. Earlier operation may be warranted in such patients.

Objectives. This study examined the performance of the 62-lead body surface electrocardiogram (ECG) in identifying the site of origin of ventricular tachycardia in patients with a previous myocardial infarction. Background. Because the accuracy of ECG localization of ventricular tachycardia using standard 12-lead recordings is restricted to the identification of rather large ventricular areas, application of multiple torso lead recordings may augment the resolving power of the surface ECG and result in more discrete localization of arrhythmogenic foci. Methods. Thirty-two patients were selected for electrophysiologically guided ablative therapy for drug-resistant postinfarction ventricular tachycardia. In these patients, QRS integral maps of distinct monomorphic ventricular tachycardia configurations were correlated with a previously generated infarct-specific reference data base of paced QRS integral maps. Each paced pattern in the data base corresponded with ectopic endocardial impulse formation at 1 of 18 or 22 discrete segments of the left ventricle with a previous anterior or inferior myocardial infarction, respectively. Electrocardiographic localization was compared with the results obtained during intraoperative or catheter endocardial activation sequence mapping. Results. Body surface mapping was performed during 101 distinct ventricular tachycardia configurations. Compared with the activation mapping data that were acquired in 64 of 101 ventricular tachycardias, body surface mapping identified the correct segment of origin in 40 (62%) of 64 tachycardias, a segment adjacent to the segment where the arrhythmia actually originated in 19 (30%) of 64 tachycardias and a segment disparate from the actual segment of origin in 5 (8%) of 64 tachycardias. With respect to infarct location, the segment of origin was correctly identified in 28 (60%) of 47 ventricular tachycardias in patients with anterior, 7 (70%) of 10 tachycardias ia patients with inferior and 5 (71%) of 7 tachycardias in patients with combined anterior and inferior myocardial infarction. Conclusions. This study shows that body surface mapping enables precise localization of the origin of postinfarction ventricular tachycardia in 62% and regional approximation in 30% of tachycardias. The multiple-lead ECG nay be used to guide and shorten catheter-based mapping procedures during ventricular tachycardia and to provide relevant information on the origin of tachycardias that cannot be mapped with conventional single-site mapping techniques because of unfavorable characteristics.

BACKGROUND The purpose of this study was to assess the value of body surface mapping and the standard 12-lead ECG in localizing the site of origin of postinfarction ventricular tachycardia (VT) during endocardial pace mapping of the left ventricle. METHODS AND RESULTS Simultaneous recordings of 62-lead body surface QRS integral maps and scalar 12-lead ECG tracings were obtained in 16 patients with prior myocardial infarction during a total of 26 distinct VT configurations and during subsequent left ventricular catheter pace mapping at 9 to 24 different endocardial sites. Anatomic pacing site locations were computed by means of a biplane cineradiographic method and plotted on a polar projection of the left ventricle. The QRS integral map and the QRS complexes of the 12 standard leads of each VT morphology obtained in a particular patient were compared independently with the different paced QRS integral maps and paced QRS complexes of the 12-lead ECG generated in that same patient. The stimulus site locations of the best matching paced QRS integral map and paced QRS complexes of the 12-lead ECG were indicated on the polar projection and subsequently compared with the endocardial location of the corresponding site of VT origin identified during intraoperative (surgical ablation) or catheter activation sequence mapping (catheter ablation). The localization resolution of pace mapping was established separately for each electrocardiographic technique by computing the size of endocardial areas with similar morphological features of the QRS complex. Pace mapping advocated with body surface mapping or the 12-lead ECG enabled adequate reproduction of the VT QRS morphology in 24 of 26 VTs (92%) and 25 of 26 VTs (96%), respectively. Activation sequence mapping identified the site of origin in 12 of 26 previously observed VT configurations (46%). Ten and 11 VTs were localized by activation sequence mapping and pace mapping combined with body surface mapping or the 12-lead ECG, respectively. Pace mapping applied with body surface mapping identified the site of origin correctly (distance < or = 2 cm) in 8 of 10 compared VTs (80%); an adjacent site (distance between 2 and 4 cm) or a disparate site (distance > or = 4 cm) was identified in the remaining 2 of 10 VTs (20%). Pace mapping used with the 12-lead ECG localized the site of origin correctly in 2 of 11 VTs (18%); the site of origin was identified correctly next to an additional adjacent site in 5 of 11 VTs (55%); and an adjacent site or a disparate site was found in 1 of 11 VTs (9%) and 2 of 11 VTs (18%), respectively. The difference in localization accuracy of both electrocardiographic techniques was statistically significant (P = .02). The mean size of endocardial areas where a comparable QRS morphology was obtained during pace mapping was 6.0 +/- 4.5 cm2 with the application of body surface mapping and 15.1 +/- 12.0 cm2 with the use of the 12-lead ECG. CONCLUSIONS These results demonstrate that application of the 62-lead instead of the 12-lead ECG during endocardial pace mapping enhances the localization resolution of this mapping technique and enables more precise identification of the site of arrhythmogenesis in the majority of compared postinfarction VT episodes.

OBJECTIVES. The present study was designed to evaluate a new method for assessing coronary collateral flow and resistance in conscious humans. BACKGROUND. Earlier pathomorphologic and invasive studies have indicated that collateral vessels are important for salvage of myocardium at risk in acute myocardial infarction. Only a few clinical studies have attempted to express the development of the collateral vascular bed in terms of flow or resistance. METHODS. Angiography and flow velocity measurements of the contralateral coronary artery were performed in 38 patients undergoing coronary angioplasty for one-vessel disease. Coronary flow velocity was assessed by zero-crossing frequency analysis in 37 patients and, additionally, by fast Fourier transform spectral analysis in 23. Collateral flow was determined by the decrease of flow velocity after balloon deflation. Mean aortic pressure and coronary wedge pressure were assessed for calculation of collateral vascular resistance. RESULTS. Angiography of the contralateral artery during balloon inflation revealed the presence of collateral vessels in 26 patients (recruitable collateral vessels in 19). Fast Fourier transform spectral analysis demonstrated a significant transient increase of flow velocity during brief coronary occlusion in 15 patients with collateral vessels compared with 8 patients without collateral vessels (4.8 +/- 1.3% vs. 23.4 +/- 17.2%, p < 0.001). A transient increase in flow velocity (> 10%) was less evident by zero-crossing frequency analysis than by fast Fourier transform spectral analysis (sensitivity 8% vs. 87%). The relative resistance of the collateral vascular bed was significantly reduced when collateral vessels were present during coronary occlusion (4.4 +/- 3.8 vs. 16.9 +/- 4.6, p < 0.001). Furthermore, electrocardiographic signs of ischemia were less present in those 15 patients with collateral vessels (p < 0.05). CONCLUSIONS. The beneficial effect of collateral vessels during brief coronary occlusion is exerted by a significant increase of flow in the contralateral artery in combination with a reduced resistance in the collateral vascular bed. The method presented is capable of expressing the development of the collateral vascular bed in terms of flow and resistance

To improve electrocardiographic localization of the site of origin of ectopic left ventricular (LV) impulse formation in the heart with prior myocardial infarction, 62-lead body surface QRS integral maps were studied during LV pacing at a total of 221 endocardial sites in 14 patients with previous anterior (AMI), inferior (IMI), lateral (LMI), or anterior and inferior (AMI/IMI) myocardial infarction. The anatomic location of each pacing site was computed using digitized biplane fluoroscopic images and plotted on standardized LV endocardial polar projections. A data base of characteristic AMI and IMI mean QRS integral maps was developed after visually selecting subgroups with nearly identical QRS integral morphology from the ectopic activation sequences produced at 110 sites in eight patients with AMI and at 66 sites in four patients with IMI. Intrasubgroup pattern uniformity and intersubgroup pattern variability were statistically verified. The endocardial pacing site locations belonging to each AMI and IMI subgroup were depicted as segments on the respective LV polar projections. In patients with AMI, a total of 18 typical mean QRS integral patterns were obtained, whereas 22 different mean total QRS integral patterns showing more substantial intersubgroup variation were acquired in patients with IMI. Posterolateral regions exhibited a relatively low electrocardiographic sensitivity (six AMI and five IMI patterns) as compared with anteroseptal regions (12 AMI and 17 IMI patterns). Total QRS integral patterns obtained at 24 sites in one patient with LMI were largely compatible with the IMI mean total QRS integral patterns, whereas the majority of total QRS integral patterns acquired at 21 sites in one patient with AMI/IMI corresponded with the AMI mean total QRS integral patterns. The results show that total body surface QRS integral maps generated during LV pacing in patients with prior myocardial infarction cluster by pattern and that each QRS integral pattern is related to a circumscribed endocardial segment of ectopic impulse formation. The relation between a given QRS integral pattern and the position and size of the corresponding paced segment is dependent on infarct location. The present infarct-specific data base of characteristic total body surface QRS integral patterns provides a clinical tool to obtain detailed electrocardiographic localization of ventricular arrhythmias in patients with previous myocardial infarction.

In patients after cardiac surgery, hypotension, defined as a mean arterial pressure less than 65 mmHg despite adequate filling pressures and positive inotropic medication, poses a problem. In addition, it is often difficult to determine whether these patients have suffered irreversible myocardial injury or if they are likely to recover. In this study, left and right ventricular function, as assessed by transesophageal echocardiography (TEE), was related to mortality both (1) quantitatively, using fractional area change (FAC), and (2) qualitatively, using a segmental wall motion analysis, which assigned a score to myocardial wall segments, in order to determine whether this technique can be used to predict survival. Mortality rate was very high in patients with biventricular and especially right ventricular failure (FAC less than 35%). Left and right ventricular wall motion abnormality indices were significantly better in survivors compared to nonsurvivors, but no distinct cut-off value could be determined. A wall motion index derived from only 6 segments at the mid-papillary muscle level was found to be as reliable as one based on 16 segments of the entire left ventricle. Thus, TEE provided information about the degree of left and right ventricular dysfunction by using a single cross-section at the papillary muscle level. It identified patients at high risk of death, ie, those with compromised right and biventricular function.

Because it is sometimes difficult to determine the cause of hypotension in patients after cardiac operations, we assessed the value of transesophageal echocardiography in this respect, and we studied 60 consecutive patients who had hypotension despite positive inotropic medication and, in some patients, mechanical support. Echocardiographic diagnoses were compared with diagnoses based on hemodynamic parameters. Follow-up examinations were completed in all patients to confirm the final diagnoses. Echocardiographic signs of hypovolemia were present in 14 patients, tamponade in six, left ventricular failure in 16, right ventricular failure in 11, and biventricular failure in eight. Echocardiographic examination proved to be inconclusive in five patients. Comparison with hemodynamic parameters showed agreement on diagnoses (hypovolemia versus tamponade versus cardiac failure) in 30 patients (50%). Echocardiography correctly identified two patients with tamponade and six with hypovolemia; these conditions were not suspected by standard hemodynamic data; in five patients unnecessary reoperation was prevented, although hemodynamic values were suggestive of tamponade. Echocardiography also identified subcategories of patients at high risk of death (those with signs of right ventricular and biventricular failure). These findings suggest that transesophageal echocardiography performed on patients after cardiac operations, at the bedside in the intensive care unit, can readily elucidate the cause of hypotension in the large majority of patients and is a valuable adjunct to hemodynamic evaluation in patient management. Furthermore, it appears to be possible to identify subcategories of high-risk patients, based on these echocardiographic findings.

Doppler echocardiographic evaluation of the prosthetic valve function is usually performed at rest, although this situation is not representative for patients' daily activities. Therefore, a symptom-limited Master 2-step test was performed in 61 asymptomatic patients with normal left ventricular function. No adequate Doppler signals were obtained in 5 of 61 patients (8%) within 60 second after termination of exercise. In patients with aortic valve prostheses (n = 24), heart rate increased from 74 +/- 10 to 105 +/- 18 beats/min, the maximal instantaneous gradient from 44 (range 22 to 90) to 68 (range 28 to 165) mm Hg (r = 0.89) and the mean gradient from 24 (range 12 to 50) to 39 (range 18 to 100) mm Hg (r = 0.90). In 6 of 11 patients with a maximal flow velocity ratio between the left ventricular outflow tract and the aortic valve prosthesis less than or equal to 0.25, the mean gradient increased to a value greater than or equal to 50 mm Hg after exercise, whereas in patients with a ratio of greater than or equal to 0.25, this never occurred. In patients with mitral valve prostheses (n = 39), heart rate increased from 80 +/- 12 to 116 +/- 14 beats/min and mean gradient from 6 (range 3 to 10) to 14 (range 6 to 25) mm Hg (r = 0.59). The correlation of the mean diastolic pressure gradient after exercise with pressure half-time was 0.66. Systolic pulmonary artery pressure at rest and after exercise could be determined in 22 of 39 patients (56%) and increased from 34 (range 20 to 70) to 57 (range 35 to 110) mm Hg. It is concluded that the response to exercise can, to a large extent, be inferred from Doppler parameters at rest, particularly in patients with aortic valve prostheses. The clinical implication of the high gradients found in some asymptomatic patients in the present study should be elucidated by follow-up studies.

To determine the factors that influence the presence of collateral vessels during coronary occlusion, we performed standardized contrast injection of the contralateral coronary artery in 58 consecutive patients, without previous myocardial infarction, undergoing percutaneous transluminal coronary angioplasty for 1-vessel disease (left anterior descending artery in 45, right coronary artery: in 10 and left circumflex artery in 3). The presence of collateral vessels during coronary occlusion, defined as partial or complete epicardial opacification by collateral vessels of the vessel dilated, was related to clinical, angiographic and electrocardiographic parameters. The angiographic appearance of collateral vessels during balloon inflation showed a weak, although statistically significant, correlation to the percent diameter stenosis before angioplasty (r = 0.28; p = 0.03) and the duration of angina (r = 0.37; p = 0.004). By combining lesion severity with the duration of angina, collateral vessels during coronary occlusion were particularly related to a lesion severity greater than or equal to 70% and duration of angina greater than or equal to 3 months (p less than 0.001). Furthermore, the presence of collateral vessels was associated with an absence of ST-segment shift (greater than or equal to 1 mm) during 1 minute of coronary occlusion (p less than 0.001).

To assess the relation between early Indium-111 monoclonal antimyosin antibody scintigraphy and degree of regional asynergy on discharge, 38 patients with a first acute myocardial infarct were studied (18 anterior, 20 inferoposterior infarctions). In 21 patients thrombolytic therapy was administered. On the first day of myocardial infarction, 80 MBq Indium-111 Antimyosin was injected. Planar images, anterior, lateral and left anterior oblique, were made 24 hours later. Localized myocardial uptake was present in 37/38 patients, and was evaluated for Count Density Index (count density of infarct zone/left lung count density) in the left anterior oblique images, which displayed the infarct zone well. Regional asynergy on discharge was evaluated by cross-sectional echocardiography and defined mild (hypokinesia) or severe (akinesia or dyskinesia). Count density index was significantly lower in 15 patients with mild asynergy, compared with 22 patients with severe asynergy (1.61 +/- 0.25 vs. 2.42 +/- 0.40, p less than 0.001). This difference was present in both patient groups treated with or without thrombolysis. We conclude that early count density index, reflecting the amount of local necrosis, is highly correlated to the ultimate degree of wall motion impairment.

OBJECTIVE--To determine the long term effects of relaxation therapy on 24 hour ambulatory intra-arterial blood pressure in patients with mild untreated and uncomplicated hypertension. DESIGN--Four week screening period followed by randomisation to receive either relaxation therapy or non-specific counselling for one year. Ambulatory intra-arterial blood pressure was measured before and after treatment. SETTING--Outpatient clinic in Amsterdam's university hospital. SUBJECTS--35 Subjects aged 20-60 who were being treated by general practitioners for hypertension but were referred to take part in the study. At three consecutive screening visits all subjects had a diastolic blood pressure without treatment of 95-110 mm Hg. Subjects were excluded if they had damaged target organs, secondary hypertension, diabetes mellitus, a cholesterol concentration greater than 8 mmol/l, or a history of malignant hypertension. INTERVENTIONS--The group allocated to relaxation therapy was trained for eight weeks (one hour a week) in muscle relaxation, yoga exercises, and stress management and continued exercising twice daily for one year with monthly visits to the clinic. The control group had the same attendance schedule but had no training and were requested just to sit and relax twice a day. All subjects were asked not to change their diet or physical activity. MAIN OUTCOME MEASURE--Changes in ambulatory intra-arterial blood pressure after one year of relaxation therapy or non-specific counselling. RESULTS--Mean urinary sodium excretion, serum concentration of cholesterol, and body weight did not change in either group. Diastolic pressures measured by sphygmomanometry were 2 and 3 mm Hg lower in subjects in the relaxation group and control group respectively at the one year follow up compared with initial readings. The mean diastolic ambulatory intra-arterial pressure during the daytime had not changed after one year in either group, but small treatment effects could not be excluded: the mean change for the relaxation group was -1 mm Hg (95% confidence interval -6 to 3.9 mm Hg) and for the control group -0.4 mm Hg (-5.3 to 4.6 mm Hg). Mean ambulatory pressure in the evening also had not changed over the year, and in both groups nighttime pressure was 5 mm Hg higher. The variability in blood pressure was the same at both measurements. CONCLUSIONS--Relaxation therapy was an ineffective method of lowering 24 hour blood pressure, being no more beneficial than non-specific advice, support, and reassurance--themselves ineffective as a treatment for hypertension.

Using a radiotransparent electrode array, body surface maps (BSMs) were constructed based on simultaneous recordings from 62 leads on the entire thorax before, during, and after balloon inflation during percutaneous transluminal coronary angioplasty (PTCA). Twenty-five patients were studied, and 30 angioplasties were performed; 20 patients had one-vessel disease, and five patients had two-vessel disease. In total, 15 dilations in the left anterior descending artery (LAD), seven in the right coronary artery (RCA), and eight in the left circumflex artery (LCx) were studied. For each patient, the BSM and the QRS integral map before, during, and after the inflation was compared by subtraction of recordings "during-minus-before" inflation and "before-minus-after" inflation. The subtraction was performed on the results of the QRS integral maps. The conclusions derived from the inspection of the BSMs and the difference maps show specific changes in the QRS complex during ischemia related to the corresponding ischemic segment in 21 of 25 patients in the three groups. An area of positive potentials remained present on the BSM during dilation, indicating a depolarization wave front. For the LAD group, positive potentials were seen on the anterior thorax and, for the RCA group, on the lower part of the thorax. By subtraction analysis, these changes were extracted and presented as difference maps. For the LCx group, the BSM revealed no changes in pattern but the difference map showed a difference vector pointing in a anteroposterior direction. A regional myocardial conduction delay was hypothesized as the most likely cause for the results.

The clinical outcome and long-term follow-up of 130 consecutive patients (141 episodes) with active infective endocarditis who were treated between 1966 and 1991 were analyzed. There was a shift toward a higher proportion of referred patients (39 to 78%), patients aged > 60 years (11 to 41%) and urgent surgical treatment (11 to 44%). Medical treatment was administered in 98 patients (70%); 30-day mortality was 27%. Surgery was performed in 43 patients (30%), with an operative mortality of 26%; 9 of 14 patients (64%) who underwent operation within the first week of admission died. Patients with severe heart failure are at the highest risk for early mortality (relative risk = 21.1; 95% confidence interval 7.4-60.3). Referred patients were much more often treated surgically than were nonreferred patients (48 versus 14%) and had a lower operative mortality (24 vs 30%). Nonreferred patients were more often treated medically (86 vs 52%) and with lower mortality (19 vs 39%). The total follow-up time was 730 patient-years; only 1 patient was considered lost to follow-up. The overall cumulative 5-year and 10-year survival after hospital discharge for patients after urgent surgery were 84 +/- 7% and 53 +/- 7%, respectively, and for those after medical treatment 84 +/- 5% and 77 +/- 6%, respectively. The probability of remaining free of late events (recurrent endocarditis, late valve replacement or death) during 5 and 10 years for patients after urgent surgery was 84 +/- 7% and 53 +/- 15%, respectively, and for those after medical treatment 59 +/- 6% and 40 +/- 7%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

In long-term follow-up studies of survival after an initial event (eg, an operation) mortality from causes other than the one under study obscures the results, especially in elderly patients. In the traditional approach to the calculation of expected mortality a fictitious cohort is drawn from the general population, being matched for age, sex, and calendar time at the time of the initial event. The membership of this cohort is then kept constant from the initial event until the closing date of the study. The survival and mortality of this static cohort is then compared with that of the dynamic patient cohort to throw light on mortality from extraneous causes. This method can lead to severe bias if there is a strong correlation between the duration of observation of the patients and their age. The analysis can be improved by applying rate adjustment when calculating the background component of mortality. In this approach mortality rates from the general population are adjusted (weighted) so that the age, sex, and calendar year are at all times identical with those of each of the patients still alive and under observation. This is illustrated by means of a simplified example and a real-life one from a study at survival after aortic valve replacement. Estimation of rate-adjusted background mortality provides a framework that may put long-term survival, especially of elderly patients, in proper perspective.

As regional wall motion abnormality (RWA) is the first sign of ischaemia, transoesophageal echocardiography was evaluated as a monitoring device in 51 patients undergoing abdominal aortic surgery. Wall motion of the entire left ventricular wall (nine segments) was semiquantitatively evaluated 15 min before and after aortic cross-clamping and 3 h after declamping. In addition, limb lead II of the electrocardiogram was simultaneously recorded. At baseline, RWA was present in 16 patients (31%). New or worsened RWA 15 min after aortic cross-clamping was seen in 17 patients, of whom 11 had persistent RWA, i.e. it was still present 3 h after declamping. This was associated in seven patients with enzymatically documented myocardial infarction. Only one infarct patient demonstrated ST segment changes of more than 1 mm. Thus, a single electrocardiographic surface lead is insensitive for perioperative myocardial ischaemia detection. Furthermore, new and/or worsened RWA after aortic cross-clamping, which persists until 3 h after declamping, is, to a considerable degree, associated with perioperative infarction.

Long-term reproducibility of Doppler recordings made by the same investigator using the same ultrasound equipment was determined in 50 clinically stable patients. The mean interval between the first and second examination was 16 +/- 7 months. In 90% of the 33 patients with aortic prostheses, the relative difference between the first and second examination was less than 16% (mean value 9.1%) for the maximum instantaneous gradient and less than 17% (mean value 7.4%) for the mean gradient; the relative difference was less than 20% (mean value 8.5%) for the maximum flow velocity in the left ventricular outflow tract and less than 24% (mean value 10.8) for the maximum flow velocity ratio. In 90% of the 25 patients with mitral prostheses, the absolute difference between the first and second examination was less than 3 mmHg for the maximum instantaneous gradient, less than 2.5 mmHg for the mean gradient, and less than 20 msec for the pressure half-time. We conclude that long-term reproducibility of Doppler echocardiographic characteristics of prosthetic valve function is good as far as transprosthetic gradients or pressure half-time are concerned but is less so for maximum flow velocity in the left ventricular outflow tract and the maximum flow velocity ratio. Changes beyond the aforementioned values may represent a real change in prosthetic valve function.

Management recommendations based on Doppler echocardiographic examination and cardiac catheterization were compared in a prospective study in 100 consecutive patients who were admitted for evaluation and treatment of suspected valvular heart disease during 1988. Management recommendations were provided independently after both Doppler echocardiography and cardiac catheterization by different and blinded investigators. Criteria for severe (clinically significant) and moderate to mild (insignificant) valvular lesions and management recommendations were agreed on in advance. There was disagreement on the severity of aortic stenosis based on the aortic valve area and maximum instantaneous pressure gradient in 1 of 54 patients, which resulted in differing management recommendations. Mitral stenosis was severe (valve area ≤ 1 cm 2 ) at Doppler echocardiography but not at cardiac catheterization in 5 of 14 patients. Because pulmonary artery pressure increase during exercise at cardiac catheterization also suggested severe obstruction, management recommendations were similar. There was a potentially significant disagreement on the severity of aortic regurgitation in 9 of 76 patients and of mitral regurgitation in 14 of 90 patients; however, this did not produce differing management recommendations because with most patients coexistent valvular lesions or an impaired ventricular function mainly determined the ultimate management decision. Although of good quality, Doppler echocardiographic examination was nonconclusive for clinical decision-making in 15% of the study population because of uncertainty about the severity of mitral regurgitation or aortic regurgitation or because of problems in assessing the degree of left ventricular dysfunction in patients with severe regurgitation. Nonsuspected coronary artery disease (>50% luminal narrowing) was present in 25% of patients with isolated mitral valve disease, in only 6% of patients with isolated aortic valve disease, and in 14% of patients with combined aortic and mitral valve disease. Thus although Doppler echocardiography was less reliable in isolated aortic or mitral regurgitation, management recommendations could be provided in the large majority (85%) of patients, and Doppler echocardiography showed disagreement with cardiac catheterization in only one patient. The decision to perform selective coronary angiography should be individualized.

The immediate and long-term prognosis of patients with acute myocardial infarction depends mainly on the extent of the infarcted myocardium. Although some prognostic information can be obtained from the M-mode echocardiogram by measurements of left ventricular internal dimensions and an abnormality in mitral valve closure [1], or by mapping the extent of left ventricular asynergy using multiple transducer positions [2], M-mode echocardiography remains a poor method for quantitating the involved myocardium due to the restricted field of vision.

To determine the clinical outcome and the long-term results of a second coronary artery bypass operation, we studied preoperative clinical status and catheterization data in 200 consecutive patients over a 9-year period (1979 to 1987) (mean follow up time 34 months, maximum 120). The study group included 169 men and 31 women (mean age 58.4 years [7% > 70 years]). Sixty-four percent of patients had severe angina (New York Heart Association class IV), 70% had 3-vessel coronary artery disease and 21% had poor left ventricular function. Reoperation was performed after a mean interval of 58 months after the first procedure. A mean of 3.3 distal anastomoses was placed. The operative mortality rate (30 days) was 7.5%, with additional cardiac morbidity (myocardial infarction, heart failure) in 11.5% of patients. Multivariate analysis showed an increased risk in women (risk ratio 3.6) and in patients with poor left ventricular function (risk ratio 3.1). The cumulative 5-year survival rate was estimated at 84%, with a rate of 77% for patients with poor left ventricular function (difference not significant). The probability of remaining free of a cardiac-related event (myocardial infarction, angioplasty, third operation, cardiac death) was 64% for 5 years. At the end of follow-up, 79% of the surviving patients were in New York Heart Association class I or II and nearly 50% of patients in the fifth year after the reoperation had good functional status. It is concluded that a reoperation is effective but carries an increased, immediate, operative risk. Late survival is good and most patients will be free of cardiac events and be in a good clinical condition in the first 5 years.

The value of simultaneous 62-lead electrocardiographic recordings in localizing the site of origin of ectopic ventricular activation in a structurally normal heart was assessed by examining body surface QRS integral maps in 12 patients during left and right ventricular (LV and RV) pacing at 182 distinct endocardial sites. A data base of 38 characteristic mean integral maps was composed after visually selecting subgroups with nearly identical total QRS integral morphology and numerically evaluating intrasubgroup pattern uniformity and intersubgroup pattern variability. Corresponding endocardial pacing site locations were computed by a biplane cineradiographic method and outlined as segments on a standardized LV and RV polar projection. LV pacing resulted in 25 markedly different mean total QRS integral patterns, showing higher electrocardiographic sensitivity for anteroseptal (18 patterns) compared with posterolateral regions (seven patterns). RV pacing demonstrated 13 mean total QRS integral patterns, exhibiting less intersubgroup variation and comparatively low electrocardiographic sensitivity for the basal anterior and outflow regions. Comparison of LV with RV pacing revealed that QRS configurations produced at LV apical and LV midseptal sites closely resembled QRS configurations generated at RV apical, RV septal, and RV anterior sites, respectively. Total QRS time integral amplitudes showed considerable intrasubgroup variation but permitted global differentiation of spatially similar QRS patterns obtained during pacing at LV and RV sites. This study demonstrates that the QRS pattern of the total body surface electrocardiogram allows discrimination among 38 different LV and RV segments of ectopic endocardial impulse formation in patients with normal cardiac anatomy.

Left ventricular short-axis cross-sections at the level of the papillary muscles and transmitral flow were obtained with transesophageal echocardiography during percutaneous transluminal coronary angioplasty (PTCA) in 15 patients who had received anesthesia and who all demonstrated new areas of or more severe wall motion abnormality 10.2 +/- 4.3 seconds after initiation of balloon inflation. Both systolic (percentage area reduction and ejection fraction of the ischemic segment) and diastolic (early to atrial peak flow ratio and time velocity integral) function parameters and end-systolic wall stress changed significantly during PTCA. These changes were most profound during PTCA of the left anterior descending artery than they were during PTCA of the right coronary artery. Systolic and diastolic dysfunction are therefore invariably linked during transient ischemia, and PTCA of the left anterior descending artery consistently produced more profound dysfunction.

The predictive value of the left ventricular spatial flow pattern for thrombus formation was determined in 62 patients with acute myocardial infarction. A normal flow pattern by pulsed Doppler echocardiography was characterized by 1) simultaneous onset of blood motion at the mitral valve and apical level, and 2) a discontinuous Doppler signal along the lateral wall and interventricular septum. The flow pattern was assessed by these criteria, within 24 h after the onset of complaints and after 6 and 12 weeks. In 46 of the 62 patients, a normal flow pattern was found at the first examination; none of these 46 patients developed a thrombus during the study period. An abnormal flow pattern was seen at the first examination in 16 patients; this pattern normalized during follow-up in 6 patients, none of whom developed a thrombus. In the other 10 patients the abnormal flow pattern persisted, and 7 of these developed a thrombus. These findings suggest that a normal left ventricular flow pattern in the setting of acute myocardial infarction is not associated with subsequent thrombus formation. This observation may be of importance if anticoagulation is considered.

More than fifty years ago Tennant and Wiggers were the first to demonstrate that ‘the ventricular zone affected by ligation of a large coronary branch not only appears cyanotic and dilated, but that it seems to alter in its mode of contraction’ [1].

To assess reduction of infarct size by therapeutic intervention, a high predictive accuracy is mandatory. The CK release in the circulation (CKr) was studied in 12 consecutive patients after uncomplicated myocardial infarction, admitted within 5 h after onset of symptoms. Despite improvement of existing methods, such as a more frequent sampling, CK-MB determination instead of total CK determination and use of a gamma-exponential instead of a log-normal curvefitting technique, the correlation between CK, predicted from measurements within 7 h after the start of CK rise and CKr calculated after completion of the CK curve remained poor. Computer simulations were done to investigate measurement errors as a cause of this failure. Normally distributed noise, with standard deviations ranging from 0.2% to 8.0% of peak CK-MB, was added to the first points of an ideal gamma-exponential CK-MB curve and predictions were made from these "noisy" points. A small noise already produced a great variation in prediction: 0.8% noise resulted in a deviation of predicted CKr from calculated CKrranging from -20 to + 6%. It is concluded that adequate prediction of infarct size from serial CK determinations in the first 7 h after onset of the CK rise must fail if the precision of the biochemical determination is not less than 0.4%.

1. The influence of supine rest on the blood pressure response to standing and 70° head-up tilt was studied in detail for the first 30 s after the change of posture. 2. Following 20 min of supine rest, the active transition to standing was accompanied by an immediate increase in systolic pressure of 29 ± 6 mmHg (mean ± sem). This was followed by large fluctuations in systolic pressure: to −28 ± 2 mmHg below control after 7 s and to 22 ± 2 mmHg above control after 22 s (17 mmHg in excess of the systolic pressure level after head-up tilt). 3. Following 1 min of supine rest, there was no difference in the immediate increase in systolic pressure. However, the magnitude of the subsequent changes was significantly diminished. 4. With head-up tilt the immediate increase in blood pressure was absent and afterwards small changes were found that were also significantly influenced by the period of prior rest. 5. Taken in conjunction with earlier studies, the following mechanisms are suggested. The immediate blood pressure increase resulted from compression of arteries by the contracting postural muscles. The subsequent blood pressure fall was caused by at least two mechanisms: (a) the fall was predominantly of reflex origin, because the immediate pressure increase stimulated the systemic baroreceptors; (b) supine rest possibly augmented the translocation of blood from the thorax which contributed, approx. 5 s from standing, to the reflex fall of blood pressure.

Left ventricular inflow was studied with pulsed Doppler echocardiography in 12 normals and 12 patients with a dilated left ventricle as a result of ischemic heart disease. To study the influence of left ventricular relaxation on both the transmitral and apical diastolic flow patterns, we applied range ambiguity. This provides simultaneous display of Doppler shifts obtained at different depths. The diastolic Doppler shift curves at the mitral valve and apical level in normals had the same time of onset, whereas there was an apparent time delay in the patients with heart disease (range 160-360 ms). This might be caused by absence of a normal apical wall motion in these patients.

In 60 consecutive patients with acute myocardial infarction early Doppler echocardiographic measurements of ventricular systolic and diastolic function were obtained and correlated with the degree of heart failure during the subsequent clinical course. Transmitral flow (early to atrial peak flow velocity ratio [E/A], systolic function measurements (maximal velocity at aortic anulus level [Vmax]), and time velocity integral (TVI) were obtained, as well as an "outflow tract ratio" (OTR), that is, measurement of the functional length of the left ventricular outflow tract. Spatial apical flow pattern was assessed with the sample volume positioned near the lateral wall and interventricular septum and by the simultaneous recording of apical and transmitral flow with a high pulse repetition frequency. Mean values of both E/A and systolic measurements of the entire group were used as cutoff values to identify patients with absent or mild heart failure defined as Killip I and II. E/A greater than 0.96 had a low specificity (45%) and positive predictive value (70%). Systolic function: Vmax greater than 0.66 m/sec, TVI greater than 12.6 cm, and OTR less than 0.48 had a specificity of 86%, 93%, and 93%, respectively, and a positive predictive value of 91%, 96%, and 96%. Normal spatial apical flow patterns demonstrated a specificity of 84% and positive predictive value of 91% to identify patients with infarctions who have a subsequent mild clinical course. Thus in contrast to E/A, both systolic function measurements and spatial apical flow patterns may identify on admission patients with a subsequent mild clinical course.

In a prospective, controlled study, the influence of strenuous physical exercise on plasma total cholesterol, HDL cholesterol, apolipoprotein A-I, total triglycerides and fatty acid composition of adipose tissue was studied during 7 months of training in 15 senior oarsmen and 21 controls matched for age, smoking and drinking habits. Dietary intake was monitored. At the start of the study there were no differences in lipid parameters and adipose tissue composition between oarsmen and controls. A significant decrease in total cholesterol and total triglycerides and an increase in HDL cholesterol and apolipoprotein A-I was noted in the oarsmen after only 2 weeks of training. Body weight remained stable but skin-fold thicknesses decreased. Food consumption increased considerably but diet composition remained unchanged Nevertheless the fatty acid pattern of adipose tissue changed significantly, as a result of altered preferential endogenous fatty acid synthesis and/or fatty acid oxidation. Since lipid parameters and adipose tissue composition were equal in oarsmen and controls before the start of the training, it is concluded that the changes induced by exercise only last for the duration of the training period.

1. The initial heart rate (HR) response evoked by standing, 70° head-up tilt, handgrip and contraction of abdominal and leg muscles was analysed in diabetic patients with autonomic neuropathy and in matched controls. 2. in healthy subjects standing induced an immediate, large, HR increase lasting 20 s that far exceeded the small HR rise induced by tilt. The HR response with handgrip and to contraction of abdominal and leg muscles was strikingly similar for the first 5 s to the HR increase after standing. 3. in diabetic patients handgrip and standing induced a small HR increase starting after 2–3 s. Contraction of abdominal and leg muscles evoked little or no HR changes. The HR rise after tilt up was delayed by 10 s compared with healthy controls. 4. It is concluded that the circulatory response to active and passive changes of posture differs fundamentally. Standing and handgrip are superior to head-up tilt as a test for vagal HR control. An abrupt and large HR increase after standing excludes cardiac parasympathetic neuropathy. A modified response, however, may be due to afferent as well as to efferent lesions, e.g. in muscle afferents or in vagal afferents from cardiopulmonary receptors.

Blood flow recordings made by 2 dimensional Doppler echocardiography can sometimes be understood more easily than conventional Doppler recordings, because of the anatomical 2 dimensional presentation. In contrast, signal processing has become more complicated and requires more explanation. In 2 dimensional Doppler echocardiography the analog ultrasonic signal received by the transducer is converted into an audible signal, which next is digitized and analyzed for its mean frequency and variance. Data collection and processing require application of multigating and high speed frequency analysis, generally based upon autocorrelation. Some artifacts may be perceived, such as color reversal due to aliasing, deceptively colored tissue surfaces due to beam motion, and wall motion ghost signals due to multiple reflections. Color flow imaging is appropriate for a rapid scan of the heart cavities to detect and roughly evaluate flow abnormalities. Quantification is still accomplished by switching to conventional Doppler mode.

The present study was designed to evaluate the myocardial protective effect of nicardipine (NIC) in patients with normal left ventricular (LV) function (control vs. NIC treatment group) and impaired LV function (control vs. NIC treatment group) during extracorporeal circulation for coronary artery surgery. NIC infusions were begun approximately 12 min before aortic cross clamping (AoX) at an infusion rate of 5 micrograms.kg-1.min-1 and maintained for 10 min. Prior to AoX an additional bolus of NIC 5 mg was given. Coronary hemodynamics, myocardial metabolic parameters (continuous thermodilution), and regional LV function (two-dimensional transesophageal echocardiography) were measured. At 15 min after discontinuation of AoX, lactate production was found in the two control groups but not in the two NIC treatment groups. In the control groups, lactate production returned to extraction at sternal closure. At that time regional area ejection fraction (RAEF) had significantly improved in both groups with impaired LV function compared with postintubation (baseline) values. In NIC-treated patients with impaired LV function, however, the percentage improvement in RAEF was significantly greater than that in the control groups. Between the groups, there were no differences in the number of patients requiring inotropic support, pacing, and/or diuretics after bypass or postoperatively. There were no significant differences in postoperative creatine kinase myocardial band release or in the incidence of dysrhythmias, myocardial infarction, or mortality. The results of the present study suggest that NIC iv may be used to provide additional myocardial protection during extracorporeal circulation. In addition, in NIC-treated patients with compromised LV function, this may be associated with a more apparent improvement in RAEF than that seen in nontreated patients.

We have investigated the relationship between vagal and sympathetic lesions in 62 diabetic patients and compared the results with those from 37 healthy subjects. Vagal function was assessed by heart rate changes with forced breathing. Sympathetic control was measured by the heart rate and blood pressure changes after standing and the concomitant plasma catecholamine response. The integrity of the postganglionic sympathetic neuron was evaluated separately by testing sudomotor function. Impaired sympathetic control was found only in 15 diabetic patients with severely impaired or absent vagal heart rate control. In 12 patients the chief abnormalities consisted of a delayed and diminished heart rate increase, an excessive fall in systolic blood pressure (greater than 20 mmHg) in combination with an abnormally small noradrenaline increment (less than 120 ng/l) and a lesion of the postganglionic sympathetic neuron. Three patients with severely impaired parasympathetic heart rate control in combination with an intact postganglionic sympathetic neuron demonstrated a large noradrenaline increase on standing (greater than 700 ng/l). Measurement of vagal heart rate control and testing of sudomotor function makes it possible to classify a spectrum of abnormal cardiovascular responses to standing in diabetic patients.

Pulsed Doppler echocardiography was performed in nine patients with spontaneous intracavitary dynamic echoes, revealing a circular flow pattern. All patients had a severely dilated left ventricle as a result of ischemic heart disease. The sample volume was placed in the apical four-chamber view near the lateral wall and near the interventricular septum, halfway between the mitral valve anulus and apex. A continuous (i.e., during both systole and diastole) positive signal was recorded near the lateral wall and a continuous negative signal at the interventricular septum. This indicates flow continuously toward the transducer along the lateral wall and away from the transducer along the interventricular septum. This is consistent with the circular flow pattern, as demonstrated by the spontaneous intracavitary dynamic echoes. In 22 normal volunteers a positive prominent shift was recorded during diastole near the lateral wall and either a negative (nine of 22) or no (13 of 22) shift at all during systole. Near the interventricular septum a negative systolic shift followed by a positive, early-diastolic shift was consistently recorded. In the large majority (18 of 22) negative waves were recorded during middle and late diastole. A continuous positive or negative Doppler signal was consistently absent in healthy subjects. The angle between the proximal part of the interventricular septum and the anterior mitral valve leaflet during maximal early diastolic opening in the patients was 74 +/- 4.8 degrees (mean +/- SD), which may give rise to a preferential eccentric inflow and the maintenance of the circular apical flow pattern.

In 21 patients treated with thrombolysis for acute myocardial infarction (AMI), the degree of myocardial uptake of indium-111 monoclonal antimyosin antibodies injected within 24 hours after onset of AMI was compared with the degree and extent of regional asynergy on admission and discharge, as assessed by 2-dimensional echocardiography. On the first day of AMI, 80 MBq of indium-111 antimyosin was injected and planar images were made 24 hours later. Indium-111 antimyosin uptake was evaluated for count density index (count density of infarct zone/left lung count density) in the left anterior oblique projection, in which the infarction zone was well displayed in all patients. Using 2-dimensional echocardiography, the left ventricle was divided into 13 segments and evaluated for regional asynergy, which was considered severe (akinesia or dyskinesia) or mild (hypokinesia). The extent of regional asynergy was measured by the number of asynergic segments. All 21 patients had severe regional asynergy on admission. Nine of 21 showed only mild regional asynergy on discharge and 12 of 21 had persistent severe regional asynergy in at least 1 segment. The count density index was significantly lower in patients with mild regional asynergy on discharge compared with patients with severe regional asynergy (1.63 +/- 0.27 vs 2.50 +/- 0.42, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

More than fifty years ago, Tennant and Wiggers [1] were the first to demonstrate that “the ventricular zone affected by ligation of a large coronary branch not only appears cyanotic and dilated, but that it seems to alter in its mode of contraction”. Since then, the function of ischemic and nonischemic myocardium has been studied extensively in animal models by a variety of techniques [2–6], including M-mode and two-dimensional echocardiography. Similar data in humans on the effect of transient ischemia on left ventricular function have been limited to observations during spontaneous or provoked attacks of angina pectoris. Using two-dimensional echocardiography, Gerson et al. [7] demonstrated in a patient with Prinzmetal’s angina, akinesia of the previously normally contracting left ventricular posterior wall during a provoked attack of pain.

In a randomized controlled study examining the value of an intramuscular injection of lidocaine in the prehospitalization phase of suspected acute myocardial infarction, paramedics used an automatic injector to administer 400 mg of the drug into the patient's deltoid muscle before transport to the hospital. In a 33-month period, 7026 patients with acute chest pain were seen. Of the 6024 patients randomized (2987 to the lidocaine group and 3037 to the control group), 1935 (32 per cent) proved to have an acute myocardial infarction. In the entire 60-minute period of observation by continuous electrocardiography, primary ventricular fibrillation was observed in 8 treated and 17 control patients (P = 0.08). However, from 15 minutes after randomization onward, when plasma lidocaine levels were in the therapeutic range, only 2 cases of ventricular fibrillation occurred in the treated group, as compared with 12 in the control group (P less than 0.01). Ventricular tachycardia terminated a mean of 10 minutes after injection in six of nine lidocaine-treated patients with acute myocardial infarction but in none of five control patients with infarction (P less than 0.02). Mean plasma lidocaine levels were 3 micrograms per milliliter 11 to 20 minutes after injection in 369 consecutive patients. In 65 patients, levels were below 2 micrograms per milliliter, and in 15 patients, levels were above 6 micrograms per milliliter. Side effects were rare and did not contribute to mortality. We conclude that intramuscular lidocaine may be useful if given by a paramedic, another person, or the patient himself when acute myocardial infarction is suspected outside the hospital.

Two-dimensional transesophageal echocardiography was used to evaluate the effect of coronary revascularization on regional myocardial function in 30 patients. Cross-sections at the level of the papillary muscles were obtained 15 minutes after intubation, 15 minutes after sternal closure, and 6 and 12 hours later, in the intensive care unit. Regional myocardial function of eight segmental areas was obtained using a floating axis system. The segments were allocated to one of four conditions, depending on baseline regional area ejection fraction (RAEF): condition I) RAEF0%; condition II) RAEF = 0% to 25%; condition III) RAEF = 26% to 50%; or condition IV) RAEF50% (normal). Compared to baseline values (postinduction), RAEF changed after sternal closure in condition I from -10.4% +/- 5.4% to 17.6% +/- 10.3% (P.01), in condition II from 14.3% +/- 6.1% to 30.7% +/- 7.8% (P.01), and in condition III from 35.0% +/- 6.1% to 50.4% +/- 6.3% (P.01). In condition IV there was no significant change in RAEF. Further improvement of RAEF in conditions I, II, and III was not seen in the intensive care unit. Thus, preoperative normal regional myocardial function was not affected by coronary revascularization, and dysfunctioning myocardium frequently improved immediately after revascularization.

This study determined the relative value of transthoracic and transesophageal color Doppler flow imaging to systolic flow patterns in the left atrium in different types of mechanical prostheses in the mitral valve. Thirty-nine patients were investigated. Based on clinical findings, 36 of 39 patients had normal prosthetic valve function. Seventeen patients were interrogated within a few days after surgery. Systolic regurgitant jets in the left atrium were absent in all patients by both transthorack pulsed and color Doppler flow imaging. Using transthorack continuous wave Doppler, however, jets were demonstrated in 8 of 39 patients (21%). Transesophageal color Doppler flow imaging demonstrated systoic regurgitant jets originating from the prosthesis in all patients. Tilting disc valves showed jets during the entire systole (closure and leakage backflow). Each type of prosthesis generated a specific jet pattern. Pathologic regurgitant jets were crescent-shaped, more extensive and turbulent than jets caused by normal closure and leakage backflow. Thus, transthorack color Doppler flow imaging is not sensitive for detecting regurgitant jets in mechanical prostheses in the mitral valve. All mechanical prostheses show a specific jet pattern, which should be helpful when transesophageal echocardiography is used to identify pathologic backflow.

We explored in 43 healthy subjects the afferent mechanisms of the initial heart rate response to standing by comparing free standing, 70 degrees head-up tilt, handgrip, and contraction of abdominal and leg muscles. The results indicate the following. 1) Standing evokes an immediate, large, bimodal increase of heart rate (HR) of about 20 s duration that far exceeds the gradual HR rise induced by 70 degrees head-up tilt. 2) The immediate HR increase with active standing is due to the exercise reflex and results in a first peak about 3 s after standing briskly. 3) The secondary, more gradual HR increase after 5 s of standing and the subsequent rapid decrease of HR between about 12 and 20 s corresponds through the baroreceptor reflex with a striking fall, recovery, and sometimes overshoot of arterial pressure. 4) The maximum HR increase found after about 12 s of standing is augmented and delayed after rest. 5) The time course of the initial HR response is not modified by physical training. We conclude that active and passive changes of posture result in fundamentally different cardiovascular effects for about 20 s and that "central command," muscle receptors, high-pressure receptors, low-pressure receptors, and the plasma catecholamine level are probably all involved in the initial HR response to standing.

We studied nine freshmen and 14 senior oarsmen undergraduates during seven months of training and compared them with 17 age and sex-matched sedentary control subjects in order to assess the influence of heavy physical exercise on cardiac dimensions and maximal oxygen uptake. Standard M-mode echocardiographic techniques were used. At the start of the season senior oarsmen had a greater left ventricular end-diastolic dimension, and a thicker interventricular septum and posterior left ventricular wall than control subjects and freshmen oarsmen. The two latter groups did not differ from each other. During the training period there was a slight and gradual increase in left ventricular end-diastolic dimension, and interventricular septum and posterior wall thickness in freshmen. In seniors only left ventricular end-diastolic dimension increased significantly. Maximal oxygen uptake showed a distinct increase between the fourth and seventh month during the period of intensive rowing training. There was no relation between echocardiographic variables and maximal oxygen uptake. A combination of heavy dynamic and static exercise can thus lead to significant changes in both left ventricular wall thickness and chamber size within months. Echocardiographic variables measured at rest cannot be used as a suitable index of performance capacity.

Left ventricular thrombus complicating myocardial infarction was diagnosed by two-dimensional echocardiography in 119 patients. The infarct site was anterior in 98 patients and inferior in 11. Systemic embolism occurred in 26 patients (stroke in 18, lower limb embolism in 7 and mesenteric embolism in 1). A protruding configuration of the thrombus was more common in the patients with embolism than in those without (23 [88%] of 26 versus 17 [18%] of 93) (p less than 0.01). Free mobility of the thrombus was found in 15 (58%) of 26 and 3 (3%) of 93 cases, respectively (p less than 0.01). In predicting embolism, protruding thrombus configuration had a sensitivity of 88% and a specificity of 82%, and positive and negative predictive accuracy was 57 and 96%, respectively. For free mobility of the thrombus, sensitivity was 58%, specificity 97%, positive predictive accuracy 85% and negative predictive accuracy 89%. In the 46 patients whose echocardiogram was obtained during the hospital admission for the index infarct, repeat echocardiograms were obtained during oral anticoagulant therapy. Twelve of these 46 patients had embolism and 2 of the 12 died. In seven of these patients, full dose oral anticoagulant therapy had been given before embolism occurred and in five it was started after an embolic event. The thrombus decreased in size or disappeared in six patients; in four the thrombus showed no change, and in two of these four emboli recurred despite anticoagulation. It is concluded that two-dimensional echocardiography may help delineate the embolic potential of left ventricular thrombus complicating myocardial infarction and may be of value in weighing the benefits and disadvantages of oral anticoagulant therapy.

In order to evaluate biochemical and circulatory parameters during purely mental stress, 20 healthy medical students were studied before, during and at the end of an important written medical examination. Plasma catecholamines and diastolic blood pressure rose significantly during the examination, whereas systolic blood pressure did not change and heart rate declined. Continuous ECG recording in 12 of the subjects showed a high peak in heart rate at the start of the examination, quickly followed by a rapid decline to values seen on the previous day. It is suggested that in mental stress without physical effort, the enhanced sympathetic activity triggers an increase in parasympathetic activity which overrides the circulatory effects of the former. 1981 Association for the Publication of the Journal of Internal Medicine

In order to study myocardial and clinical events during transient coronary occlusion in humans, two-dimensional echocardiography was continuously performed in 15 patients undergoing 49 balloon inflations during percutaneous transluminal coronary angioplasty (PTCA). Transient segmental asynergy developed in all patients 8 +/- 3 seconds after balloon inflation and returned to baseline 19 +/- 8 seconds after balloon deflation. Segmental dyskinesis was seen in only 8 of 11 patients undergoing PTCA of the left anterior descending artery (LAD). A wall motion score, based on degree of asynergy of 13 segments of the left ventricle, was significantly higher during LAD than during right coronary artery inflation (7.9 +/- 1.3 vs 4.0 +/- 1.4, p less than 0.01). Left ventricular size index increased significantly during balloon inflation, from 179 +/- 9 to 196 +/- 10 mm (p less than 0.01). Four patients developed transient ST segment changes in the extremity leads of the ECG and five patients had angina pectoris. The very first sign of ischemia in three patients, who developed all of these symptoms together, was consistently asynergy, followed by ECG changes, and last, angina pectoris. Thus during PTCA, transient asynergy and left ventricular dilatation develop, which are often clinically silent.

Calcium antagonists influence cardiovascular hemodynamics by 3 actions: peripheral arterial dilatation, coronary arterial dilatation and negative inotropic effect. The net hemodynamic effects vary depending on the relative strength of each action. Intravenous administration of the new compound nicardipine, a dihydropyridine derivative with calcium antagonist activity that is chemically related to nifedipine, induced a marked reduction of systemic vascular resistance in patients with and without β blockade. This was accompanied by an increase in cardiac output and left ventricular ejection fraction. In addition, end-diastolic pressure, peak (+) dP dt and dP dt measured at a developed pressure of 40 mm Hg and normalized for this pressure remained unchanged. The time constant of isovolumetric pressure drop during the first 40 ms also decreased. Intravenous administration of nicardipine prevented a marked increase in end-diastolic pressure during exercise, and augmented left ventricular ejection fraction in chronic heart failure. At doses producing similar increases in coronary sinus blood flow, intracoronary administration of nicardipine, unlike nifedipine, has little effect on left ventricular contractility and end-diastolic pressure. Nicardipine is a powerful systemic vasodilator with minimal effects on myocardial inotropic state, even in patients with compromised left ventricular function and patients receiving β blocker therapy.

Transesophageal 2-dimensional echocardiography was performed in 21 patients soon after uncomplicated coronary artery bypass grafting to determine the mechanism of positive end-expiratory pressure (PEEP) ventilation-induced decreased cardiac output. End-diastolic and end-systolic short-axis area and percent area reduction of right and left ventricles were determined during 5-cm H2O stepwise increments of PEEP ventilation. Simultaneously, cardiac output and right- and left-sided hemodynamic values were determined. Cardiac output, mean arterial pressure and end-diastolic area of both ventricles gradually decreased, and right and left atrial and pulmonary arterial pressures (mainstem and capillary wedge) increased. Left ventricular end-systolic area did not change, whereas right ventricular area decreased. Percent area reduction of both ventricles decreased (p less than 0.01). Thus, decrease in cardiac output during PEEP ventilation is primarily caused by decrease of preload rather than compromised contractility.