Effect of the undisturbed pericardium on left ventricular size and performance during acute volume loading

Studies in instrumented dogs have suggested that the pericardium alters left ventricular diastolic pressure-volume relations and thus may influence systolic performance. However, the instrumentation used in these studies disrupts the pericardium and may have influenced the results. We therefore studied five conscious dogs by methods not traumatic to the pericardium, before and after pericardiectomy. Although heart rate and left ventricular systolic and end-diastolic pressures were not different before or after pericardiectomy, either at rest or during volume loading, end-diastolic volume measured by biplane two-dimensional echocardiography increased post pericardiectomy at rest from 38 ± 4 (SE) to 61 ± 4 ml (p < 0.05) and during volume loading from 68 ± 5 to 79 ± 5 ml (p < 0.005). After pericardiectomy, ejection fraction was unchanged, but the peak value of the first derivative of left ventricular systolic pressure ($\text{dP}\text{dt}$) increased significantly at rest from 17 ± 2 to 26 ± 4.0 × 10² mm Hg/sec. We conclude that pericardiectomy shifts the left ventricular end-diastolic pressure-volume curve to the right and increases the systolic isovolumic index of $\text{dP}\text{dt}$ in the basal state.     

Left ventricular dimensions and function during exercise in dogs with chronic right ventricular pressure overload

Left ventricular (LV) dimensions and shortening at rest and during treadmill exercise were examined before and after 4 weeks of pulmonary artery (PA) constriction in 6 conscious dogs. The dogs were preinstrumented with LV and right ventricular (RV) catheters, an LV micromanometer, a PA inflatable cuff occluder and ultrasonic crystals to measure an LV anteroposterior, a septal-lateral, an apex-base and a free wall segment chord. With PA constriction, RV pressures increased from $\text{49 ±}\text{4}\text{2}\text{± 1 mm}$ Hg (systolic/end-diastolic) to $\text{104 ±}\text{5}\text{2}\text{± 1}$ at rest and from $\text{71 ±}\text{9}\text{2}\text{± 1}\text{to}\text{133 ±}\text{8}\text{14}\text{± 2}$ at peak exercise (mean ± standard error of the mean). Heart rate, LV pressure and LV dP/dt were similar before and after RV pressure overload at rest and with exercise. During exercise at control, systolic shortening increased significantly in all chords. With chronic PA constriction at rest, shortening of all chords also remained normal despite decreases in end-diastolic dimensions, which were most marked in the septal-lateral chord (23% decrease, p <0.01). However, during exercise in the presence of RV pressure overload, septal-lateral shortening decreased 46% (p <0.01) despite increases in systolic shortening in the other chords similar to the control response. Therefore, although LV function at rest in chronic RV pressure overload is normal, exercise may induce regional abnormalities of LV contraction that appear to be mediated by a reduced contribution of the ventricular septum to LV ejection.     

Left ventricular function in systole and diastole in constrictive pericarditis

Left ventricular function was studied in systole and diastole in 30 patients with constrictive pericarditis. Left ventricular end-diastolic volume was used to divide the patients into three arbitrary groups: severe constriction (EDV < 25 ml./M.²), moderate constriction (EDV 25 to 50 ml./M.²), and mild constriction (EDV > 50 ml./M.²).The patients had high ventricular diastolic and venous filling pressures (mean LVEDP = 23 ± 7 mm. Hg, mean RVEDP = 20 ± 7 mm. Hg). Measurements related to absolute fiber shortening (stroke index, stroke work index, and left ventricular ejection rate) were reduced and linearly related to the degree of constriction as assessed by the end-diastolic volume.Measurements of relative fiber shortening or lengthening (ejection and filling fraction and circumferential fiber shortening) were normal despite great reduction in ventricular volumes.Velocity measurements, peak LV $\text{dp}\text{dt}$ and mean velocity of circumferential fiber shortening were normal or slightly reduced.These changes were reflected in the systolic time interval measurements pre-ejection phase, left ventricular ejection time, and the ratio $\text{PEP}\text{LVET}$.Diastolic function of the ventricle was abnormal; the distensibility index of the ventriculo-pericardial system ($\text{ΔV}\text{ΔP}$) was low and the passive elastic modulus in-increased. The change in compliance correlated with the degree of constriction and there was a linear relationship between compliance and EDV.The ventricle was underloaded despite the high filling pressure and stroke work index was reduced; extrinsic compression raised the diastolic pressure and reduced left ventricular volumes.     

Effects of chronic oral quinidine on left ventricular performance

We studied the effects of 10 to 14 days of oral quinidine administration (200 mg every 8 hrs) on left ventricular (LV) $\text{dP}\text{dt}$ max and shortening fraction (%ΔD) in seve preinstrumented consclous dogs in the resting state, during atrial pacing at 120 bpm, and during an acute pressure load produced by intravenous phenylephrine. Dogs were studied before, during, and after oral quinidine administration with control measurements varying by < 10%. In the resting state, heart rate (85 ± 6 SEM vs 88 ± 7 bpm), LV end-diastolic pressure (7.2 ± 1.4 vs 6.7 ± 1.1 mm Hg), LV end-diastolic diameter (39.6 ± 3.2 vs 38.9 ± 2.7) did not differ (p > 0.05) before or during quinidine, respectively. During atrial pacing LV $\text{dP}\text{dt}$ increased similarly during the control and quinidine periods (+ 13 and + 11%), and %ΔD decreased equally (?26% and ?21%) during phenylephrine infusion off and on quinidine. Thus chronic oral quinidine administration in clinically therapeutic doses (serum quinidine levels 2.3 to 7.5 μg/ml) produced no depression in LV performance at rest or during an acute pressure load.     

Acute effects of ethanol on myocardial blood flow in the nonischemic and ischemic heart

To determine the effects of ethanol on myocardial blood flow in the non-ischemic and ischemic heart, coronary blood flow was measured with radionuclide-tagged microspheres in the anesthetized dog before and after intravenous administration of 1.7 g/kg body weight of ethanol. In non-ischemic dogs, at an average peak blood ethanol level of 225 ± 8 mg/dl (mean ± standard error of the mean), left atrial pressure increased from 5.7 ± 0.6 to 7.7 ± 0.8 mm Hg (p <0.01) and heart rate slowed from 179 ± 8 to 171 ± 8 min^?1 (p <0.001) but mean aortic pressure and cardiac output were unchanged. Average myocardial blood flow increased from 122 ± 5 to 143 ± 8 ml/min per 100 g (p <0.001). In dogs given ethanol after coronary occlusion, at an average peak blood ethanol level of 201 ± 13 mg/dl, left atrlal pressure increased from 6.3 ± 0.6 to 7.4 ± 1.4 mm Hg (p <0.05) but there was no significant change in heart rate, mean aortic pressure or peak positive first derivative of left ventricular pressure ($\text{dP}\text{dt}$). In these dogs, there was a significant change (F = 6.47, p <0.001) in the distribution of myocardial blood flow. In the nonischemic zone, blood flow increased from 118 ± 7 to 148 ± 14 ml/min per 100 g (p <0.005), whereas in the ischemie zone it declined from 30 ± 6 to 20 ± 5 ml/min per 100 g (p <0.02). Myocardial tissue demonstrating myocardial perfusion equal to or greater than 80 percent of preligation levels showed a significant increment of blood flow after ethanol; by contrast, myocardial tissue having blood flow levels equal to or less than 60 percent of preligation levels showed a significant decline in blood flow.Thus, ethanol increases coronary blood flow in the nonischemic myocardium. However, in the acutely ischemic heart, ethanol produces an unfavorable redistribution of myocardial blood flow with flow in the non-ischemic myocardium increasing, at least in part, at the expense of blood flow to ischemic myocardium, producing in effect a “coronary steal.”     

Effects of nitroglycerin on supine and upright exercise in mitral stenosis

Resting, supine, and upright exercise hemodynamics were studied in 11 patients with pure or predominant mitral stenosis before and after 0.4 mg sublingual nitroglycerin. Resting mean pulmonary wedge pressure was reduced from 27 ± 1.6 to 21 ± 1.6 mm Hg (p < 0.001), while mean cardiac index (2.98 ± 0.40 vs 2.68 ± 0.30 cc/min/m²; NS) and mean heart rate (82 ± 4.4 vs 87 ± 6.7 bpm; NS) were unchanged after nitroglycerin. Resting mean left ventricular end-diastolic pressure dropped from 11 ± 1.7 to 8 ± 1.1 mm Hg (p < 0.02) after nitroglycerin, while stroke index (37 ± 5.1 vs 32 ± 3.8 mm Hg; NS) was unchanged. Left ventricular systolic pressure fell from 122 ± 6.0 to 111 ± 3.1 mm Hg (p < 0.001) after nitroglycerin. At peak supine exercise similar qualitative changes were observed. Mean pulmonary wedge pressure was lower after nitroglycerin (43 ± 2.3 vs 36 ± 2.1 mm Hg; p < 0.02), while cardiac index (3.62 ± 0.39 vs 3.4 ± 0.26 cc/min/m²; NS) and heart rate (116 ± 7.1 vs 113 ± 4.6 bpm; NS) were not different. Left ventricular end-diastolic pressure (13 ± 1.4 vs 10 ± 1.3; NS) was slightly but not significantly reduced by nitroglycerin. Left ventricular stroke index (34 ± 3.4 vs 31 ± 2.2 mm Hg; NS) was unchanged by nitroglycerin. Left ventricular systolic pressure (137 ± 7.3 vs 127 ± 6.1 mm Hg; p < 0.02) was reduced 10 mm Hg at peak supine exercise after nitroglycerin. During upright exercise, peak heart rate (160 ± 8.1 vs 160 ± 8.0 bpm; NS) and peak systolic blood pressure (117 ± 5.7 vs 112 ± 2.8 mm Hg; NS) were not changed with nitroglycerin. Exercise duration was improved after introglycerin (5.02 ± 0.62 vs 5.66 ± 0.65 minutes; p < 0.02). Thus sublingual nitroglycerin lowers mean pulmonary wedge pressure to reduce pulmonary congestive symptoms, improves supine exercise hemodynamics, and may enhance treadmill exercise duration in some patients with pure or predominant mitral stenosis.     

Use of intra-aortic nitroglycerin in the cardiac catheterization laboratory

The purpose of this study was to determine whether nitroglycerin (NTG) injected into the ascending aorta or left ventricle would safely and effectively lower blood pressure in hypertensive patients undergoing cardiac catheterization. Fifty bolus injections of 297 ± 67 μg (mean ± SD) NTG were given to patients with a systolic blood pressure (SBP) of ?140 mm Hg (mean SBP 188 ± 20.1 mm Hg). An average drop in systolic blood pressure of 36 ± 16 mmHg (P < 0.001), diastolic blood pressure of 19 ± 7 mm Hg (P < 0.001), and left ventricular end-diastolic pressure of 4.7 ± 4 mm Hg (P = 0.001) was well tolerated in each patient. The mean time to response was 11 ± 3 sec. Intra-aortic injection of NTG is a safe and effective means to treat hypertensive patients in the cardiac catheterization laboratory. © 1995 Wiley-Liss, Inc.     

Effects of nitroglycerin on isometric exercise

Eight patients with ischemic heart disease performed isometric handgrip of five minutes' duration at 30% of their maximum voluntary contraction, before and after administration of 0.4 mg sublingual nitroglycerin (NTG). Although isometric exercise resulted in similar rise of left ventricular systolic pressure (LVSP) before and after NTG, the level of LVSP during the post NTG effort was lower. Heart rate, cardiac index, stroke index, left ventricular stroke work index, and systemic resistance were not different during the pre- and post NTG exercise. Left ventricular end-diastolic pressure rose to a significantly lower level (18.3 ± 14.4 mm Hg) during the post NTG handgrip than during the pre NTG effort (31.4 ± 17.6 mm Hg, P < 0.005). It is concluded that NTG reduces preload and afterload both at rest and during isometric exercise and improves left ventricular performance during isometric exercise.     

Alteration of left ventricular performance by left bundle branch block simulated with atrioventricular sequential pacing

The effects of atrioventricular (AV) sequential pacing-induced left bundle branch block (LBBB) on left ventricular (LV) performance were evaluated during cardiac catheterization in 9 randomly selected patients being investigated for chest pain. All patients were in normal sinus rhythm with a normal P-R interval and QRS duration. LV performance was assessed by both hemodynamic and angiographie measurements. The maximal rate of LV pressure increase (dP/dt), rate of maximal LV pressure decrease ($\text{?dP}\text{dt}$), LV end-diastolic pressure (LVEDP), end-diastolic volume (LVEDV), end-systolic volume (LVESV), stroke volume and percent ejection (EF) were measured during right atrial and AV sequential pacing at a constant pacing rate. The average pacing rate was 97 ± 3 beats/min (mean ± standard error of the mean). In each patient, both dP/dt and $\text{?}\text{dP}\text{dt}$ decreased significantly (p < 0.001) during AV sequential pacing compared with atrial pacing at the same rate, from 1,541 ± 68 to 1,319 ± 56 mm Hg/s for dP/dt and from 1,506 ± 86 to 1,276 ± 92 for $\text{?dP}\text{dt}$. LVEDP did not change significantly when atrial (17 ± 3 mm Hg) and AV sequential pacing (16 ± 2 mm Hg) were compared. Mean LVEDV did not change during atrial (135 ± 13 ml) or AV sequential pacing (137 ± 14 ml). In contrast, the LVESV during AV sequential pacing was higher by 15 ml (23 % ) (from 48 ± 10 to 63 ± 12 ml) (p < 0.001); as a result, the stroke volume was lower by 13 ml (15%) and the EF decreased by 10 %, from 66 to 56 % (?15 %).These changes in LV performance during acutely induced LBBB by AV sequential pacing as compared with atrial pacing at the same rate were independent of altered preload, because both LVEDP and LVEDV were similar during the 2 different pacing modes. Peak systolic pressure during AV sequential pacing was significantly lower than that during atrial pacing (161 ± 10 vs 145 ± 10 mm Hg, p < 0.01), and thus afterload was presumably altered during the different pacing modes. However, because the observed change in systolic pressure (afterload) was lower during AV sequential pacing, this change should improve rather than result in deterioration of ejection phase indexes. Because the opposite was observed, it is concluded the deterioration in LV function noted during AV sequential pacing must be due in part to the asynchronous pattern of ventricular activation induced by this intervention.     

Similar effects of isolated systolic and combined hypertension on left ventricular geometry and function: the LIFE study

Echocardiograms of 143 patients with isolated systolic hypertension were compared to 808 patients with combined (systolic and diastolic) hypertension. All patients met electrocardiographic criteria for left ventricular hypertrophy and were evaluated off medication. Patients with isolated systolic hypertension were older, shorter, weighed less, and were mostly women, but body mass index (BMI) was similar in both groups. Systolic blood pressure (SBP) was 172 mm Hg in isolated systolic hypertension, 174 mm Hg in combined (P = not significant). Diastolic blood pressure was 83 and 101 mm Hg, respectively (P < .001). Despite having mean arterial pressure 12 mm Hg lower than patients with combined hypertension, the group with isolated systolic hypertension had equally severe abnormalities of left ventricular mass, left ventricular geometric patterns, and measures of systolic and diastolic function. Peripheral resistance was lower and pulse pressure/stroke volume ratio (arterial stiffness index) was higher and the isovolumic relaxation time shorter in isolated systolic hypertension. Multiple regression analyses identified age, height, BMI, stress-corrected mid wall shortening, stroke volume, male gender, and systolic or mean blood pressure (but not isolated systolic hypertension) as independent correlates of left ventricular mass. Relative wall thickness was independently associated with isolated systolic hypertension (P = .001) in addition to mean pressure and other covariates. The present results add support to the concept that systolic blood pressure (SBP) is a stronger determinant than diastolic pressure of cardiac target organ damage in hypertension.     

The Effects of Simvastatin on Left Ventricular Hypertrophy and Left Ventricular Function in Patients with Essential Hypertension

This study is to evaluate the effects of Simvastatin on left ventricular hypertrophy and left ventricular function in patients with essential hypertension. Untreated or noncompliance with drug treatment patients with simple essential hypertension were treated with a therapy on the basis of using Telmisartan to decrease blood pressure (BP). There were 237 patients who had essential hypertension combined with left ventricular hypertrophy as diagnosed by echocardiography, taken after their BPs were decreased to meet the values of the standard normal. Among them, there were only 41 out of the original 237 patients, 17.3%, who had simple essential hypertension combined with left ventricular hypertrophy without any other co-existing disease. They were the patients selected for this study. All patients were randomly, indiscriminately divided into two groups: one was the control group (Group T), treated with the Telmisartan-based monotherapy; the other was the target group (Group TS), treated with the Telmisartan-based plus simvastatin therapy. The changes of left ventricular hypertrophy and left ventricular function were rediagnosed by echocardiography after 1 year. The results we obtained from this study were as follows: (i) The average BPs at the beginning of the study, of simple essential hypertension combined with left ventricular hypertrophy, were high levels (systolic blood pressure (SBP) 189.21 ± 19.91 mm Hg, diastolic blood pressure 101.40 ± 16.92 mm Hg). (ii) The Telmisartan-based plus simvastatin therapy was significantly effective in lowering the SBP (128.26 ± 9.33 mm Hg vs. 139.22 ± 16.34 mm Hg). (iii) After the 1-year treatment, the parameters of left ventricular hypertrophy in both groups were improved. Compared to group T, there were no differences in the characteristics of the subjects, including interventricular septum, left ventricular mass, left ventricular mass index, ejection fraction, left atrium inner diameter at baseline. The patients’ interventricular septum (Group TS 10.30 ± 1.80 mm vs. Group T 10.99 ± 1.68 mm, P < .05), LVM (Group TS 177.43 ± 65.40 g vs. Group T 181.28 ± 65.09 g, P < .05), and LVMI (Group TS 100.97 ± 37.33 g/m² vs. Group T 106.54 ± 27.95 g/m², P < .05), all dropped more prominently (P < .05) in group TS; the ejection fraction rose more remarkably in group TS (Group TS: 57.50 ± 16.41% to 65.43 ± 11.60%, P < .01 while showing no change in Group T); the left ventricular hypertrophy reversed more significantly and the left ventricular systolic function improved more. (iv) The left atrium inner diameter of Group TS decreased (P < .01), the ratio of E/A, which indicates the left ventricular diastolic function, continued to drop further, showing no change to the trend of left ventricular diastolic function declination. Patients who have hypertension with left ventricular hypertrophy usually suffer other accompanying diseases at the same time. Telmisartan-based plus Simvastatin treatment can significantly reduce SBP, reverse left ventricular hypertrophy, improve the left ventricular systolic function, but it has no effect on reversing the left ventricular diastolic function. This experiment indicated that Simvastatin can reverse left ventricular hypertrophy and improve left systolic function.     

Beneficial effect of amrinone on myocardial oxygen consumption during acute left ventricular failure in dogs

In 11 dogs ischemic left ventricular failure characterized by a 30 percent reduction In cardiac output and a left ventricular end-dlastolic pressure of 18 mm Hg or more was produced by proximal occlusion of the left anterior descending coronary artery followed by serial occlusions of the distal left circumflex coronary artery. Administration of amrlnone In an Intravenous bolus injection followed by a constant Infusion produced Improvements in cardiac output (from 1.62 ± 0.50 to 2.19 ± 0.52 Itters/min [mean ± standarddeviation], p <0.05), left ventricular end-dlastolic pressure (from 21.6 ± 3.5 to 11.0 ± 5.4 mm Hg, p <0.05) and peak positive rate of rise of left ventricular pressure [dP/dt](from 1,264 ± 241 to 1,800 ± 458 mm Hg·^?1, p <0.05). These Improvements were maintained throughout the 20 minute period of therapy. No significant alteration in heart rate or arterial pressure was noted. In parallel with the hemodynamic improvement myocardial oxygen consumption improved to 0.094 ± 0.05 and 0.092 ± 0.04 vol·^?1?^?1 after 2 and 20 minutes; respectively, of amrinone compared with 0.124 ± 0.05 during left ventricular failure (both <0.05). The effects of amrinone on left ventricular failure are due to augmented contractility and mild systemic vasodllatation. The reduction in myocardial oxygen consumption during amrlnone-treated left ventricular failure presumably results from a reduction in ventricular wall tension that more than offsets the effect of an Increase in contractility.     

Regression of left ventricular hypertrophy in patients with essential hypertension: Results of 6 month treatment with indapamide

Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular morbidity in hypertensive patients. The effects of diuretics on LVH have raised controversies, but recent studies suggest that diuretics are able to reduce LVH in hypertensive patients, mainly through a reduction in ventricular diameter.The present multicenter open study was designed to test the effects of indapamide, a widely used nonthiazide diuretic, on LVH in patients with essential hypertension. Patients had to have mild-to-moderate essential hypertension (supine diastolic blood pressure [sDBP] 95 to 115 mm Hg) with echocardiagraphic evidence of LVH (left ventricular mass index [LVMI] > 130 g/m² for men and > 110 g/m² for women). After a 2 week placebo run-in period, eligible patients underwent a 6 month treatment with 2.5 mg indapamide daily. All echograms were performed by the same investigator before and after 6 months of indapamide. Clinical and biological acceptability and quality of life (visual analog scale) were also studied.One hundred and thirty patients were included in the study and 112 completed the trial.Indapamide induced a significant reduction in systolic and diastolic blood pressures. Indapamide induced a marked reduction in posterior wall thickness (from 12.1 ± 2.0 to 11.2 ± 1.6 mm) and in interventricular wall thickness (from 12.7 ± 1.7 to 11.8 ± 1.9 mm; each P < .001) and a slight decrease in left ventricular diameter (P = .049). This resulted in a 13% reduction in LVMI (from 161.9 ± 37.9 to 140.7 ± 33.8 g/m², P < .001). Left ventricular fractional shortening remained unchanged. There was no significant relation between changes in LVMI and changes in systolic, diastolic, or mean blood pressure. No significant adverse clinical or biological effects were reported during the study. The increased score of the visual analog scale indicated that overall well-being was improved (P < .001).Our study indicates that indapamide, in addition to blood pressure control, is able to reduce LVH. This effect was achieved mainly through a reduction in wall thicknesses rather than in internal cavity diameter.     

Comparative efficacy of three indexes of left ventricular performance derived from pressure-volume loops in heart failure induced by tachypacing

Objectives. The purpose of this study was to serially evaluate the response and variability of the end-systolic pressure-volume relation, the left ventricular end-diastolic volume-peak positive first derivative of left ventricular pressure (dP/dt) relation and the left ventricular end-diastolic volume-stroke work relation in the development of progressive left ventricular dysfunction.Background. Evaluation of systolic performance of the failing left ventricle may be enhanced by using relatively load-insensitive measures of left ventricular performance. The end-systolic pressure-volume, left ventricular end-diastolic volume-peak positive dP/dt and left ventricular end-diastolic volume-stroke work relations adequately define left ventricular performance under multiple leading conditions, but efficacy has not been fully assessed in the failing heart, particularly in the intact circulation.Methods. Fourteen dogs underwent instrumentation and rapid pacing to heart failure. Variably loaded pressure-volume beats were produced by inferior vena cava occlusion. The dogs were evaluated at baseline and at three progressively more severe levels of left ventricular dysfunction.Results. There was a progressive increase in left ventricular volumes at end-diastole ([mean value ± SE]60 ± 28 to 73 ± 29 ml, p < 0.001) and end-systole (39 ± 19 to 61 ± 27 ml, p < 0.001) during the 3 weeks of rapid pacing and a progressive decline in peak positive dP/dt (1,631 ± 410 to 993 ± 222 nun Hg/s, p < 0.001) and ejection fraction (37 ± 8% to 16 ± 11%, p < 0.001). There was a corresponding decline in the slope of each of the three relations: for end-systolic pressure-volume, 6.3 ± 2.2 to 2.8 ± 0.7 (p < 0.05); for left ventricular end-diastolic volume-stroke work, 61.9 ± 9,1 to 26.5 ± 2.4 (p < 0.05); and for left ventricular end-diastolic volume-peak positive dP/dt, 47.1 ± 13.6 to 20.31 ± 6.8 (p < 0.05). There was also a corresponding increase in position volumes: for end-systolic pressure-volume, 33.6 ± 3.9 to 61.2 ± 6.6 ml (p < 0.05); for left ventricular end-diastolic volume-stroke work, 46.2 ± 3.6 to 89.3 ± 7.6 ml (p < 0.05); and for left ventricular end-diastolic volume-peak positive dP/dt, 29.1 ± 19.1 to 68.6 ± 25.9 ml (p < 0.05). The relative degree of change in each of the three relations was similar as more severe heart failure developed. The coefficients of variation for position were significantly less than the variation for slopes. The response of volume intercepts was heterogeneous. For left ventricular end-diastolic volume-stroke work, the intercept increased as ventricular performance decreased. The intercept of the end-systolic pressure-volume relation was significantly more variable than the left ventricular end-diastolic volume-stroke work relation and did not change with progressive heart failure. The intercept for left ventricular end-diastolic volume-peak positive dP/dt was highly variable and showed no consistent changes as left ventricular function declined.Conclusions. All three relations consistently describe changes in left ventricular performance brought about by tachypaing. Evolution of left ventricular dysfunction causes a decline in slope and a rightward shift of these relations. The position of the relation is the most sensitive and least variable indicator of left ventricular systolic performance.     

Onset of hypertension during pregnancy is associated with long-term worse blood pressure control and adverse cardiac remodeling

Up to 20% of women with hypertensive pregnancy disorders might persist with chronic hypertension. This study compared clinical and echocardiographic features between women whose hypertension began as hypertensive pregnancy disorders (PH group) and women whose diagnosis of hypertension did not occur during pregnancy (NPH group). Fifty PH and 100 NPH women were cross–sectionally evaluated by clinical, laboratory, and echocardiography analysis, and the groups were matched by duration of hypertension. PH exhibited lower age (46.6 ± 1.4 vs. 65.3 ± 1.1 years; P < .001), but higher systolic (159.8 ± 3.9 vs. 148.0 ± 2.5 mm Hg; P = .009) and diastolic (97.1 ± 2.4 vs. 80.9 ± 1.3 mm Hg; P < .001) blood pressure than NPH, although used more antihypertensive classes (3.4 ± 0.2 vs. 2.6 ± 0.1; P < .001). Furthermore, PH showed higher left ventricular wall thickness and increased prevalence of concentric hypertrophy than NPH after adjusting for age and blood pressure. In conclusion, this study showed that PH may exhibit worse blood pressure control and adverse left ventricular remodeling compared with NPH.     

Alterations in left ventricular volumes and ejection fraction at rest and during exercise in patients with aortic regurgitation

This study was performed (1) to determine the changes in left ventricular volumes during exercise in patients with aortic regurgitation, and (2) to evaluate the importance of these alterations in characterizing left ventricular function in these patients. In 15 normal subjects (Group I) and in 17 patients with aortic regurgitation (Group II), left ventricular end-diastolic volume index, end-systolic volume index, ejection fraction and the ratio of peak systolic blood pressure to end-systolic volume index were measured at rest and during supine exercise. The patients with aortic regurgitation were classified into two groups on the basis of symptoms and chest radiographs: Group IIA, minimal or no symptoms, no cardiomegaly or pulmonary venous congestion; Group IIB, definite symptoms, with cardiomegaly and pulmonary venous congestion. Patients with aortic regurgitation had greater left ventricular end-diastolic and end-systolic volume indexes at rest and during exercise (p <0.05) than did normal subjects. During exercise, left ventricular end-diastolic volume index increased in normal subjects (53 ± 13 ml/m² [mean ± standard deviation] at rest, 67 ± 18 ml/m² during exercise, p <0.01), demonstrated a heterogeneous response in patients in Group IIA and increased in patients in Group IIB (180 ± 96 ml/m² at rest, 209 ± 102 ml/m² during exercise, p <0.05). During exercise, left ventricular end-systolic volume index decreased in normal subjects (18 ± 5 ml/m² at rest, $\text{15}\text{\$}\text{?}\text{6}$ ml/m² with exercise, p <0.01), increased in patients in Group IIB (82 ± 60 ml/m² at rest, 118 ± 93 ml/m² during exercise, p <0.05), and showed a variable response in those in Group IIA. At rest, left ventricular ejection fraction was similar in the three groups, but during exercise it increased in Group I (0.71 ± 0.07 at rest, 0.82 ± 0.07 with exercise, p <0.001), was unchanged in Group IIA and decreased in Group IIB (0.59 ± 0.15 at rest, 0.50 ± 0.16 during exercise, p <0.05). During exercise, there was an inverse relation between changes in left ventricular ejection fraction and endsystolic volume, but no relation between changes in end-diastolic volume and ejection fraction. Changes in the systolic pressure-volume ratio provided no more information than changes in end-systolic volume alone. Thus, abnormal alterations in left ventricular volumes occur during exercise in patients with aortic regurgitation and may be helpful in the further characterization of left ventricular performance in these patients.     

Effect of amlodipine on hemodynamic and endocrine responses to mental stress

Little is known about the effects of antihypertensive drugs on hemodynamic responses to mental stress. We studied 24 patients with mild-to-moderate hypertension in a double-blind random-sequence crossover study comparing placebo with amlodipine titrated up from 5 to 10 mg daily. After 1 month of treatment, the subjects performed 20 min of a frustrating cognitive task. At baseline before task, amlodipine significantly reduced systolic pressure (128.9 ± 8.2 mm Hg v 140.3 ± 10.7 mm Hg, P < .001), diastolic pressure (81.7 ± 7.7 mm Hg v 90 ± 7.5 mm Hg, P < .001), and total peripheral resistance (37.5 ± 15 v 45.6 ± 23.7 mm Hg/L/min, P < .05), while elevating baseline norepinephrine levels (2286 ± 731 pmol/L v 1788 ± 546 pmol/L, P < .001).Blood pressure during the stress task was significantly less with amlodipine than with placebo (systolic 142.3 ± 12.3 mm Hg v 150.9 ± 14.6 mm Hg, P < .001; diastolic 87.9 ± 8.4 mm Hg v 97.7 ± 9.3 mm Hg, P < .001), whereas norepinephrine was significantly higher (2754 ± 1007 pmol/L v 1970 ± 740 pmol/L, P < .001).There were no significant differences in cardiac output, plasma lipids or lipoproteins, or markers of platelet activation. Heart rate increased significantly during stress, but there was no significant difference between amlodipine and placebo either at baseline or during stress. Our conclusion is that amlodipine reduces blood pressure at baseline and during mental stress, but raises basal and stress-related plasma catecholamines. This finding may have implications for the recent controversy over the safety of calcium channel antagonists, and suggests the potential relevance of combining amlodipine with adrenergic blockers.     

Left ventricular structural and functional characteristics in patients with renovascular hypertension,primary aldosteronism and essential hypertension

To investigate the effect of different etiologies of hypertension on left ventricular structure and function, we compared echocardiographic findings in 10 patients with renovascular hypertension (35 ± 9 years), 10 patients with primary aldosteronism (42 ± 9 years), and 14 patients with essential hypertension (41 ± 6 years). There were no significant differences among the three groups in age, sex, body surface area, blood pressure, interventricular septal thickness, posterior wall thickness, left ventricular end-diastolic dimension or end-systolic dimension, relative wall thickness, left ventricular mass index, or spectrum of left ventricular adaptation (concentric remodeling, concentric hypertrophy, or eccentric hypertrophy). There were no differences in systolic function or diastolic function, which was assessed in terms of the peak rate of increase in dimension normalized for left ventricular end-diastolic dimension (dD/dt/D), the relaxation time, and the relaxation time to peak velocity of lengthening among groups. Multiple regression analysis showed that the systolic blood pressure was the most important determinant of left ventricular mass index (r = 0.56, P < .01), and that left ventricular mass index was the most important determinant of relaxation time and the relaxation time to peak velocity of lengthening (r = 0.48, P < .01 and r = 0.59, P < .01, respectively). The dD/dt/D was correlated only with left ventricular end-systolic dimension (r = 0.59, P < .01). Our results suggest that blood pressure may be a strong determinant of left ventricular hypertrophy, irrespective of the etiology of hypertension, and that the degree of hypertrophy may be related to left ventricular diastolic dysfunction in hypertensive patients with normal systolic function.     

Changes in left ventricular wall dimensions during regional myocardial ischemia

The relation between changes in left ventricular wall systolic thickening and other measures of left ventricular function were studied during regional ischemia in 14 open chest pigs. A fixed decrease in coronary peak blood flow from 46 ± 5 (standard error) to 13 ± 2 ml/min was produced using a screw clamp and flow probe placed around the left anterior descending coronary artery. Myocardial wall thickness was measured with a calibrated harpoon mercury strain gauge placed through the apical portion of the left ventricle and recorded continuously with left ventricular systolic pressure, the first derivative of left ventricular pressure rise ($\text{dP}\text{dt}$) and pressure-derived peak velocity of contraction. During systole, the left ventricle thickened by 10.7 ± 2.1 percent of its total average thickness of 12.7 ± 0.7 mm. Within 6 seconds of the onset of ischemia total myocardial wall thickness decreased from 1.356 ± 0.135 to 0.592 ± 0.081 mm (P < 0.001) or to 45.2 ± 5.1 percent of the control value. During ischemia, changes were noted in both the isovolumic and the ejection phases of systole in addition to left ventricular wall thinning of 0.282 ± 0.02 mm at enddiastole. There was no significant change in left ventricular pressure or its derived values. In two experiments isolated wall thickness alternans was observed. These studies indicate that myocardial wall thickness is more sensitive than ventricular pressure as a measure of local changes in myocardial function during regional myocardial ischemia.     

Effects of nitroprusside-induced reduction of elevated preload and afterload on global and regional ventricular function in acute myocardial infarction

To evaluate the effects of nitroprusside infusion on left and right ventricular ejection fractions and left ventricular regional wall motion, radionuclide ventriculography with simultaneous hemodynamic assessment was performed before and during nitroprusside infusion in 20 patients with acute myocardial infarction complicated by left ventricular failure and/or systemic arterial hypertension. Nitroprusside produced significant reductions in pulmonary capillary wedge pressure (21 ± 6 to 13 ± 5 mm Hg; ?38%; p < 0.001), mean arterial pressure (107 ± 19 to 90 ± 13 mm Hg; ?15.9%; p < 0.001), left ventricular end-diastolic volume index (84 ± 28 to 75 ± 23 ml/m²; ?10.7%; p < 0.001), and right ventricular end-diastolic volume index (77 ± 30 to 67 ± 27 ml/m²; ?13.0% p < 0.007), and significant increases in left ventricular ejection fraction (0.32 ± 0.12 to 0.37 ± 0.13; +15.6%; p < 0.0001), right ventricular ejection fraction (0.37 ± 0.11 to 0.45 ± 0.14; +21.6%; p < 0.001), and stroke volume index (25 ± 7 to 27 ± 7 ml/beat m²; +8.0%; p < 0.03). These beneficial changes in global ventricular performance were accompanied by no change in the regional contractile function of 90% of the abnormally contracting infarct-related left ventricular segments and improved regional wall motion of 34% of noninfarcted but abnormally contracting left ventricular segments. We conclude that nitroprusside-induced reduction of elevated preload and afterload in acute myocardial infarction results in salutary effects on global ventricular function and improved regional function of noninfarcted left ventricular segments but with less prominent effects on regional function of infarcted segments.