The effects of early captopril treatment on left ventricular volumes and function in patients with and without depressed global ejection fraction after acute myocardial infarction

To determine the effects of captopril on left ventricular volumesand function in patients with and without depressed ventricularfunction following acute myocardial infarction (AMI) we studied78 patients with a first Q wave AMI and no clinical evidenceof heart failure. All patients underwent radionuclide ventriculography(RVG) on the 4th day after admission and were then randomlyassigned to receive conventional treatment alone (36 patients,control group) or with the addition of oral captopril, 25 mgthree times daily (42 patients, captopril group). RVG was repeatedone month after the baseline examination. After one month theleft ventricular ejection fraction (LVEF) significantly increasedin the captopril group (from 43.2±1.3 to 50.9±1.6%,P<0.001) and remained relatively unchanged in the controlgroup (from 47±1.3 to 49.2±1.7%, P=ns). In thecaptopril group the subgroup of patients with a baseline LVEF<45% demonstrated a significant decrease in end-systolicvolume index (ESVI) (from 53.3 ±3.2 to 42.4±2.8ml.m^–2,P<0.002) and a highly significant improvement in LVEF (from36.3±1.3 to 49.6±1.8%, P<0.00005). In the controlgroup, LVEF also increased in those in whom it was <45% (from38±1.4 to 42±2.4%, P<0.01), but the increasewas less than that in the captopril group (P<0.01), mainlydue to an increase in end-diastolic volume index (EDVI) (from78.2±4.6 to 84.6±12.3 ml.m^–2, P=ns). Inboth the captopril and control subgroups of patients with abaseline LVEF 45% there was no significant change in LVEF (from50.1±0.8 to 52.1±2.6% and 53.4±1.5 to 54.2±2.1%respectively), but there was a trend for both left ventricularvolumes to increase (EDVI: from 81.4±4.7 to 91.1±9.9ml.m^–2and 76±5.7 to 90.3±9.2 ml.m^–2; ESVI: from40.6±2.6 to 45.2 ±3.4 ml.m^–2 and 32.1±2.6to 40.1 ±3.8 ml.m^–2 respectively, all P=ns). In conclusion, our study confirmed the beneficial effect ofcaptopril on left ventricular size and function in patientswith depressed global LVEF after AMI, but there was no evidenceof a similar effect in patients with preserved global LVEF,at least during the first month of treatment.     

Effects of Atrial, Ventricular, and Atrioventricular Sequential Pacing on Coronary Flow Reserve

KOLETTIS, T.M., et al .: Effects of Atrial, Ventricular, and Atrioventricular Sequential Pacing on Coronary Flow Reserve . Experimental animal data have indicated that altered left ventricular depolarization sequence as a result of right ventricular pacing may diminish coronary blood flow in the distribution of the left anterior descending coronary artery. To further investigate this, we compared the effects of atrial, ventricular, and atrioventricular (AV) sequential pacing on coronary flow reserve. Twenty-seven patients (24 male, mean age 55 ± 7 years) with normal left anterior descending coronary arteries were studied. Coronary flow reserve was calculated as the ratio of mean flow velocity at maximal coronary vasodilatation to mean flow velocity at baseline. The study consisted of two parts. In the first part, AV sequential pacing was compared to atrial pacing at the same rate; coronary flow reserve did not differ significantly between the two pacing modes (14 patients, 4.85 ± 1.88 vs 5.47 ± 1.55, respectively, P > 0.05). In the second part, all three pacing modalities were compared; coronary flow reserve was significantly higher during ventricular compared to AV sequential pacing, but not significantly different compared to atrial pacing (3.69 ± 1.42 vs 2.90 ± 0.86 vs 3.11 ± 0.89, respectively, P < 0.05). This difference was secondary to a significant decrease in mean baseline velocity during ventricular pacing, while mean velocity during hyperemia was comparable between the three pacing modes. It is concluded that AV sequential pacing does not appear to exert a significant effect on coronary flow reserve. Ventricular pacing, however, may lower resting coronary blood velocity in some patients, without affecting maximal coronary blood velocity, resulting in a higher coronary flow reserve.     

Assessment of Time Domain and Spectral Components of Heart Rate Variability Immediately Before Ischemic ST Segment Depression Episodes

In an attempt to study autonomic function during the 5-minute period preceding ischemic ST segment depression (↓ST) episodes, we selected 138 ↓ST episodes, without preceding ↓ST during the last 15 minutes before each episode, from the Holler tapes of 35 patients with multivessel coronary artery disease. For the 5-minute period preceding each ↓ST episode, we calculated the following heart rate variability (HRV) indices; the mean RR interval (RR5), the standard deviation of all RR intervals (SD Index5), the corresponding coefficient of variation (CV5), and the natural log (Ln) of the spectral components, total power at 0.000 to 0.400 Hz (TP5), low frequency power at 0.040 to 0.150 Hz (LF5), high frequency power at 0.150 to 0.400 Hz (HF5), and the ratio of the low to high frequency power (LF5/HF5). As HRV indices of the 24-hour period, we calculated the respective RR, SD Index, CV, LnTP, LnLF, LnHF, and Ln LF/HF. RR5, SD Index5, CV5, and LnTP5 were all significantly lower than RR (t =−5.343, p = 3.7 × 10⁻⁷), SD Index (t =−19.091, p = 1.99 × 10⁻⁴⁰), CV(t -15.780, p = 1.28 × 10⁻³²), and LnTP (t =−3.210, p = 0.0016), respectively. LnHF5 was inversely correlated with the magnitude of the ↓ST; r =−0.174, P < 0.05, and CV5 was inversely correlated with the natural log (Ln) of the ischemic event duration; r =−0.183, P < 0.05. Analogous results were obtained for both the painful and silent ↓ST episodes. It is concluded that HRV is decreased during the 5-minute period preceding ↓ST episodes, and is inversely related with the magnitude and the duration of the ↓ST.     

C-AMP and ANP Levels in VVI and DDD Pacing with Different AV Delays During Daily Activity and Exercise

THEODORAKIS, G., ET AL.: C-AMP and ANP Levels in VVI and DDD Pacing with Different AV Delays During Daily Activity and Exercise. Nine patients (three males) mean age 68 ± 8 years, having complete heart block, and paced in the DDD mode were examined in VVI and DDD pacing with 100 and 150 ms atrioventricular delays (AVD) during rest and exercise. Plasma atrial natriuretic peptide (ANP) and cyclic AMP (c-AMP) were measured at rest and at peak exercise test. ANP plasma levels at rest were significantly higher in VVI pacing compared to 150 AVD (p < 0.03). On exercise, ANP release was statistically increased only in DDD with 150 ms AVD, while in WI it remained in high levels at exercise but no significant change was found (p:ns). c-AMP during rest was unchanged in any pacing mode or AVD, but on exercise DDD pacing with short AVD (100 ms) released lower c-AMP plasma levels, than at rest (p:ns). DDD pacing with long AVD (150 ms) during exercise produced statistically higher c-AMP plasma levels (p < 0.05) than at rest. Also in VVI pacing the c-AMP plasma levels were statistically higher than at rest (p < 0.02). Adrenergic activity seems to be lower during exercise in DDD pacing with shorter AVD (100 ms) than in DDD with 150 ms AVD or VVI pacing. No difference was found in c-AMP plasma levels at rest. ANP release was also found to be lower at exercise in DDD pacing with short AVD (100 ms) than in DDD with 150 ms AVD. ANP plasma levels at rest were statistically higher in VVI pacing. (PACE, Vol. 13, December, Part II 1990)     

Congestive Heart Failure and VVI Pacing Mode: Dynamic Behavior of the Dispersion of Ventricular Repolarization

Dynamic Behavior of the Dispersion of Ventricular Repolarization. The aim of this study was to evaluate the circadian variation in the spatial dispersion of ventricular repolarization in continuously paced patients with congestive heart failure (CHF). Fourteen patients (10 males, 4 females, aged 65 ± 5 years) with CHF due to dilated cardiomyopathy (DCM) and an echocardiographic ejection fraction of 28%± 3% were studied. All patients underwent AV functional RF ablation and permanent pacemaker implantation for drug refractory chronic atrial fibrillation (AF). Patients were evaluated at 1 month postimplant with a three-channel 24-hour Holter monitor, using the three plane Frank orthogonal leads (X, Y, and Z), in VVI pacing mode at 70 beats/min. For each hour, the mean value of spike-T interval dispersion of the first five beats was measured. The control group consisted of 20 patients without structural heart disease, but with AF and complete AV block, continuously paced in WI mode at 70 beats/min. The dispersion of the spike-T interval had a circadian behavior in the study population, with higher values at night and lower during the daytime. During the daytime, the mean value of spike-T interval dispersion was 39 ± 5 ms and during the nighttime it was 45 ± 7 ms (P = 0.003). Such a difference between day and night was not found in the control group (38 ± 6 ms and 40 ± 8 ms, respectively, P = NS), In the daytime period the mean value of spike-T interval dispersion of our study population was comparable to that of the control group (P = NS), while during the nighttime it was significantly higher (P = 0.0004). In conclusion, by evaluating the dispersion of ventricular repolarization in two dimensions, space and time, a circadian variation was found in paced patients with CHF due to DCM. The increased QT dispersion in these patients during the nighttime period was attributed to different effects of vagal activity in normal and abnormal myocardial areas.     

Normal coronary flow reserve in patients with mitral valve prolapse, a positive exercise test and normal coronary arteries

We studied 12 patients (eight females and four males), ages30–46 years, with echocardiographically documented mitralvalve prolapse and clinical suspicion of coronary artery disease,based on a history of chest pain (five patients), angina-likepain (three patients), a positive exercise stress electrocardiogram(12 patients) and a focally positive thallium-201 stress perfusionscan (three patients), who were referred for cardiac catheterizationand found to have normal coronary arteries. Ten patients withoutevidence of heart disease served as controls. In all mitralvalve prolapse patients, coronary flow velocity reserve wasdetermined successively in the left anterior descending, leftcircumflex and right coronary arteries as the ratio of the maximun(after intracoronary papaverine) to the resting mean coronaryflow velocity. Coronary flow reserve values were fairly similarin the mitral valve prolapse and control patients; all 12 mitralvalve prolapse patients had normal coronary flow reserve (3.5)in all three coronary arteries with no significant differencesamong the arteries tested Mean values ± 1 standard deviationof the coronary flow reserve (mitral valve prolapse vs controlpatients) were 4.7 ± 0.5 vs 4.6 ± 0.6 for theleft anterior descending, 4.6 ± 0.4 vs 4.6 ± 0.3for the left circumflex and 4. ± 0.4 vs 4.4 ±0.5 for the right coronary artery (all P=non-significant). Thesubsets of mitral valve prolapse patients with different clinical‘ischaemic’ manifestations were similar in termsof the calculated coronary flow reserve in all three major epicardialcoronary arteries. In conclusion, this study demonstrated that an inadequate regionalcoronary flow reserve does not account for the clinical manifestationsof myocardial ischaemia and positive exercise tests in patientswith mitral valve prolapse and normal coronary arteries.     

Time domain analysis of the signal averaged electrocardiogram in patients with a conduction defect or a bundle branch block

Doubts have been expressed about the clinical usefulness oftime domain analysis of the signal averaged electrocardiogramin patients with prolonged QRS complex duration. We studied147 patients using a signal averaged ECG (40–250 Hz) whoseQRS complex was longer than 100 ms. A baseline electrophysiologystudy was also performed in 128 of these patients. Seventy-sevenpatients had a minor (QRS <120 and >100 ms) conductiondefect. Thirty-seven of these 77 had either induced or spontaneoussustained ventricular tachycardia (group I) and 40 had no sustainedventricular tachycardia (group II). Seventy patients had a major(QRS120 and >100 ms) conduction defect, 44 of whom had sustainedventricular tachycardia (group A). The remaining 26 withoutthis condition formed Group B. Group I compared to group IIpatients had a longer filtered QRS duration (120.8 ±14 vs 104.5 ± 9.5 ms, P<0.001), a longer low amplitudesignal duration (41 ± 12.1 vs 31 ± 12.6 ms, P<0.0001)and a lower root mean square of the last 40 ms of the filteredQRS complex (27 ± 29.8 vs 35 ± 25.3 µV,P=ns). Group A compared to group B had a longer filtered QRSduration (157.7±20.2 vs 140.7± 15.7 ms, P<0.001),a longer low amplitude signal duration (57.3 ±24.9 vs37.8 ± 20.3 ms P<0.001) and a lower root mean squareof the last 40 ms of the filtered QRS complex (14.3 ±11.2 vs 22.0 ± 10.5 1 P<0.01). Using conventionallate potential criteria, the sensitivity and specificity ofthe signal averaged ECG for the detection of sustained ventriculartachycardia patients with a minor conduction defect were 89%and 75%, respectively. The same criteria applied to patientswith a major conduction defect were sensitive (sensitivity:87%) but non-specific (specificity: 50%). However, by usingmodified late potential criteria, such as the presence of twoof any of the following three signal averaged parameters: filteredQRS duration 145 ms, low amplitude signal duration 50 ms,root mean square of the last 40 ms of the filtered QRS complex17.5µV, we derived a non-optimal but still acceptablecombination of sensitivity (68%) and specificity (73%). We concludethat traditional late potential criteria can be applied in patientswith a minor conduction defect, but modification of these criteriais necessary to derive useful clinical information for riskstratification of patients with a QRS complex duration 120ms.     

Normal coronary flow reserve in patients with mitral valve prolapse, a positive exercise test and normal coronary arteries

We studied 12 patients (eight females and four males), ages30–46 years, with echocardiographically documented mitralvalve prolapse and clinical suspicion of coronary artery disease,based on a history of chest pain (five patients), angina-likepain (three patients), a positive exercise stress electrocardiogram(12 patients) and a focally positive thallium-201 stress perfusionscan (three patients), who were referred for cardiac catheterizationand found to have normal coronary arteries. Ten patients withoutevidence of heart disease served as controls. In all mitralvalve prolapse patients, coronary flow velocity reserve wasdetermined successively in the left anterior descending, leftcircumflex and right coronary arteries as the ratio of the maximun(after intracoronary papaverine) to the resting mean coronaryflow velocity. Coronary flow reserve values were fairly similarin the mitral valve prolapse and control patients; all 12 mitralvalve prolapse patients had normal coronary flow reserve (3·5)in all three coronary arteries with no significant differencesamong the arteries tested Mean values ± 1 standard deviationof the coronary flow reserve (mitral valve prolapse vs controlpatients) were 4·7 ± 0·5 vs 4·6± 0·6 for the left anterior descending, 4·6± 0·4 vs 4·6 ± 0·3 for theleft circumflex and 4· ± 0·4 vs 4·4± 0·5 for the right coronary artery (all P=non-significant).The subsets of mitral valve prolapse patients with differentclinical ‘ischaemic’ manifestations were similarin terms of the calculated coronary flow reserve in all threemajor epicardial coronary arteries. In conclusion, this study demonstrated that an inadequate regionalcoronary flow reserve does not account for the clinical manifestationsof myocardial ischaemia and positive exercise tests in patientswith mitral valve prolapse and normal coronary arteries.     

Echocardiographic assessment of atrial tumour size and endogeneously generated contrast imagesAn experimental study

Experimental models, in vitro and in vivo, were designed tosimulate the motion of an atrioventricular valve leaflet andan atrial tumour. Cross-sectional echocardiography was usedto investigate any changes in apparent tumour size related toits motion. Both parts of the study suggest that endogenouscontrast, due to surfaces of different acoustic densities generatedaround the rapidly moving tumour, contributes to the echo-graphicpattern of the tumour. Thus, during diastole, the echo-masscloud is greater than the real size of the tumour. The echocardiographicand actual size of the tumour may be identical only in ventricularsystole when the blood flow around the atrial tumour is greatlydecreased.