Effects of AR-L 115 BS (Sulmazol), a new cardiotonic agent, in coronary artery disease: improved ventricular wall motion, increased pump function and abolition of pacing-induced ischemia

AR-L 115 BS (Sulmazol) is a new noncatechol, nonglycosidic cardiotonic agent. In 17 patients with significant coronary artery disease, the influence of AR-L 115 BS on hemodynamics and regional wall motion was investigated under the following conditions: 1) control, 2) the immediate postpacing period without medication, and 3) the postpacing period under the peak influence of AR-L 115 BS, 2 mg/kg intravenously. During the postpacing phase without medication, all patients developed ischemia (angina, ST segment alterations, increase of mean left ventricular end-diastolic pressure from 13 to 30 mm Hg), left ventricular pump function diminished and overall regional wall motion showed a tendency to decrease (p greater than 0.05). However, during the postpacing period with AR-L 115 BS medication, ischemia was abolished (no angina; mean left ventricular end-diastolic pressure decreased to 13 mm Hg; hemodynamic variables returned to control levels and left ventricular pump function showed some improvement while overall regional wall motion showed tendencies to improve. A comparison of alterations of hemodynamics and regional wall motion during the postpacing phase without medication with those under the influence of AR-L 115 BS shows that overall left ventricular pump function and regional wall motion improved while angina and an increase in left ventricular end-diastolic pressure were prevented. It is concluded that AR-L 115 BS improves left ventricular pump function and regional wall motion in coronary artery disease without inducing ischemia, probably by means of a reduction in extravascular resistance.     

Serial exercise testing up to 6 years after coronary bypass surgery: Behavior of exercise parameters in groups with different degrees of revascularization determined by postoperative angiography

To evaluate the behavior of exercise parameters in patients with different angiographically defined degrees of revascularization, serial exercise tests were analyzed in 435 patients 1 to 6 years after coronary artery bypass grafting (CABG). All patients had undergone postoperative angiography 2 to 12 months after CABG to determine the degree of revascularization achieved. Revascularization was complete in 182 patients (all significantly stenosed arteries had patent grafts), sufficient in 176 patients (at least the dominant artery supplying the left ventricle had a patent graft) and incomplete in 57 patients (the dominant artery supplying the left ventricle had a closed graft). Twenty patients had all grafts occluded. Exercise tolerance, angina-free exercise tolerance (angina threshold), maximal double product, prevalence of ≥0.1 mV exerciseinduced S-T segment depression, and the prevalence of the combination of S-T segment depression plus angina pectoris were determined in serial exercise tests (average of 3.0 postoperative exercise tests per patient for a mean follow up of 3.5 years). Patients with complete, sufficient, and incomplete revascularization showed improvement of all exercise parameters for 6, 4, and 1 year after CABG, respectively. Patients with all grafts occluded had improvement of only some exercise parameters.Five years after CABG, exercise tolerance was improved by 24 W (p < 0.0005) and 21 W (p < 0.005) in patients with complete and sufficient revascularization, respectively, and not improved in patients with incomplete revascularization or with all grafts occluded. The angiographically determined completeness of revascularization correlates with the extent and the duration of improvement of exercise parameters after CABG.     

Cardiac reserve during isoproterenol stress in patients with aortic valve disease before and after corrective surgery

The relations between left ventricular (LV) hypertrophy as estimated by LV mass and LV function and between LV hypertrophy and cardiac reserve were evaluated in 26 patients with aortic valve disease and in nine normal patients who served as controls. Ejection fraction (EF) and mean circumferential fiber shortening rate (VCF) served as indices of LV function. Reserve force of the left ventricle was tested by ventriculography during infusion of 0.3 μg/Kg. body weight/min. isoproterenol. EF and VCF were not significantly different (p > 0.05) either at rest or during isoproterenol infusion if patients with aortic stenosis were compared to patients with aortic regurgitation having comparable LV masses. Therefore we correlated the EF and VCF to the LV mass of all patients irrespective of the type of aortic valve lesion. Poor but significant inverse correlations were found at rest between LV mass and EF (r = 0.62) and between LV mass and VCF (r = 0.57). These correlations improved considerably during isoproterenol: r = 0.84 for EF and r = 0.74 for VCF.LV function was evaluated in another six patients with aortic valve disease before and nine months after successful aortic valve replacement by Björk-Shiley prostheses. LV mass before surgery was 3.6 times control and decreased after surgery to 1.7 times control (p < 0.01) which is still significantly elevated (p < 0.05). EF and VCF which were depressed before surgery (p < 0.05, p < 0.001) normalized after surgery (p . 0.05) but were reduced during isoproterenol infusion if compared to controls (p < 0.05). Thus, stress ventriculography in aortic valve disease could demonstrate a linear decrease of cardiac reserve with increasing severity of hypertrophy when resting function was normal or depressed only slightly. Regression of hypertrophy was incomplete 9 months after correction of overload and LV function, which was depressed before surgery, normalized at rest but was impaired during stress suggesting that cardiac reserve was not fully restored.     

Effect of coronary stenosis on myocardial function, ultrastructure and aortocoronary bypass graft hemodynamics.

The relation between different degrees of stenosis of the left anterior descending coronary artery and total and regional left ventricular function, myocardial ultrastructure, flbrotic content of the myocardium and hemodynamics of graft flow was studied in 70 patients with coronary artery disease. Patients with arteriographically visible collateral supply to the obstructed vessel were excluded. The degree of stenosis (quantitative measurement of luminal obstruction) and total and regional left ventricular function were measured angiographically. Regional contractile reserve was determined from postextrasystolic angiograms. Ultrastructure and fibrotic content of the myocardium (morphometry) were determined from biopsy material taken at the time of bypass surgery from the area perfused by the left anterior descending artery. Graft flow to this artery was measured under basal conditions and after release of a 30 second graft occlusion (hyperemic response). Five groups were formed: I, no stenosis; II, stenosis of 50 to 79 percent; III, of 80 to 89 percent; IV, of 90 to 99 percent; and V, 100 percent occlusion. Patients in group II had normal values for ejection fraction, regional function and reserve, normal ultrastructure, a small degree of fibrosis and no hyperemic response after release of graft occlusion. Patients in group III had similar findings except for a significant hyperemic response. Patients in group IV had moderate depression of ejection fraction, regional function and reserve, moderate ultrastructural alterations, increased myocardial fibrosis and a high hyperemic response. Patients in group V had a severely impaired ejection fraction, absent regional function and reserve, severe cell alterations and extensive scar formation.Thus, a clear sequence of events occurs with progression of coronary stenosis: until 79 percent stenosis no significant reduction of mechanical function and myocardial structure occurs. With 80 to 89 percent stenosis, poststenotic vasodilation fully compensates for the stenosis as documented by normal mechanical function and normal myocardial structure. At 90 to 99 percent stenosis, vasodilatory compensation is inadequate: Regional function decreases, degenerative ultrastructural alterations appear and the fibrotic content of the myocardium increases. With complete occlusion, compensation is ineffective, and severe loss of function and extensive scars develop.     

Determinants of the incidence and severity of ventricular arrhythmias in aortic valve disease

The incidence of ventricular arrhythmias in patients with aortic valve disease was investigated. Twenty-four-hour ambulatory electrocardiographic recordings were obtained in 93 patients without coronary artery disease (aortic stenosis [AS], n = 38; combined AS and aortic regurgitation [AR], n = 27; and AR only, n = 28). The arrhythmias were compared with the hemodynamic findings of cardiac catheterization. Ventricular premature beats (VPB) were noted in 78 patients (84%). They were rare (< 100 VPB/22 hours) in 40 patients (43%), moderately frequent (101 to 1,000 VPB/22 hours) in 23 patients (25%), and frequent (> 1,000 VPB/22 hours) in 15 patients (16%). Multiformity was found in 47 (51%), paired VPB in 32 (34%), and ventricular tachycardia in 17 (18%) of the 93 patients studied. The occurrence of ventricular arrhythmia was not related to the type of valve lesion, to the transvalvular gradient in patients with AS, or to the degree of regurgitation in patients with AR. In contrast, the grade of arrhythmia showed a negative correlation with left ventricular ejection fraction (AS, r_s = ?0.58; AS and AR, r_s = ?0.67; AR, r_s = ?0.78; all p < 0.001) and a positive correlation with peak systolic left ventricular wall stress (AS, r_s = 0.56; AS and AR, r_s = 0.56; AR, r_s = 0.57; all p < 0.001). The frequency of VPB also showed a negative correlation with left ventricular ejection fraction (AS, r_s = ?0.63; AS and AR, r_s = ?0.65; AR, r_s = ?0.71; all p < 0.001).This study indicates that ventricular arrhythmias are present in a large number of patients with aortic valve disease. The severity of arrhythmias is strongly influenced by myocardial performance. Thus, severe arrhythmias are frequently a sign of impaired left ventricular function.     

Hemodynamic and myocardial energetic changes induced by the new cardiotonic agent,AR-L 115, in patients with coronary artery disease

AR-L 115 has been shown to improve left ventricular (LV) pump function in patients with advanced congestive cardiomyopathy by the intravenous and oral routes. Since AR-L 115 effects on myocardial oxygen consumption (MV?O₂) and coronary blood flow (CSF) are unknown, the hemodynamic, myocardial metabolic, and ECG responses to AR-L 115 (2 mg/kg bolus) were monitored at 9-, 14-, and 9-minute intervals in seven patients with coronary disease, exhibiting ischemia during pacing stress only. Maximal responses occurred at the fourteenth minute after AR-L 115. There were (average) increases in cardiac index by 30%, heart rate by 19%, CSF by 39%, MV?O₂ by 34%, and LV $\text{dp}\text{dt}$ max by 27%. There were (average) decreases in peak LV systolic pressure by 13%, LV end-diastolic pressure by 42%, systemic vascular resistance by 34%, and in coronary vascular resistance by 37%. All changes were significant (p < 0.05). Myocardial lactate extraction, stroke work index, and stroke index remained unchanged (p > 0.05). The modes increase in MV?O₂ is possibly explained by the increase in contractility being partially offset by reductions in LV preload and afterload. AR-L 115-improved LV pump function was accompanied by moderate increases in MV?O₂ and CSF but without evidence of myocardial ischemia.     

Myocardial ultrastructure in patients with chronic aortic valve disease

Light and electron microscopic observations were made on left ventricular myocardium removed at operation from 16 patients with chronic aortic valve disease. In all 16 patients most cardiac muscle cells were hypertrophid, and surrounded by small amounts of fibrous tissue. In two of the six patients with pure aortic regurgitation and in four of the five patients with combined aortic stenosis and regurgitation, cardiac muscle cells with evidence of degeneration were present in addition to hypertrophied, nondegenerated cells. Degenerated cardiac muscle cells were not observed in the six patients with predominant aortic stenosis. Cardiac muscle cells with mild degeneration showed focal myofibrillar lysis, with preferential loss of thick myofilaments, and focal proliferation of tubules of sarcoplasmic reticulum. More severely degenerated muscle cells showed a marked decrease in the numbers of myofibrils and T tubules and proliferation of sarcoplasmic reticulum or mitochondria, or both. Severely degenerated cells usually were present in areas of marked fibrosis, often were atrophic, had thickened basement membranes and had lost their intercellular connections. These findings suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with chronic aortic valve disease.     

Effect of coronary collaterals on left ventricular function at rest and during stress

The influence of coronary collateral vessels on resting left ventricular function was investigated in 87 consecutive patients with complete coronary artery occlusion of at least one of the three major coronary vessels. The morphology of coronary and collateral circulation was evaluated by coronary arteriography. Left ventricular function was assessed by biplane ejection fraction and segmental wall motion was evaluated by hemiaxes shortening. Collaterals to occluded arteries were graded as good or poor, according to the caliber of the distal vessel segment. Patients were divided into those with good collaterals (n =35), and those with poor or absent collaterals (n = 52), furthermore, these two groups were subdivided according to the location of coronary artery occlusion. Collateralized single vessel occlusions were found more frequently than collateralized multiple vessel occlusions. Ejection fraction and segmental wall motion was significantly better in well collateralized occlusions than in poorly collateralized occlusions of LAD or RC and was normal or depressed only slightly if compared to 17 patients without heart disease. In contrast, total and regional myocardial function was severely depressed in poorly collateralized LAD or RC occlusion. Ventriculography after rapid ventricular pacing was performed in 12 of 87 patients with well collateralized or poorly collateralized LAD occlusion to evaluate to what extent coronary collaterals protect anterior wall motion during increased oxygen demand. Pacing induced a drastic fall of anterior wall motion in well collateralized segments whereas no change was found in poorly collateralized segments. Reviewing clinical data of two patient groups with comparable numbers and locations of occlusions revealed in the well collateralized group more severe angina (p < 0.001) and ST-segment changes during exercise (p < 0.01) than in the poorly collateralized group. The latter showed more severe dyspnoe (p < 0.01) and more histories of previous infarctions (p < 0.001). We conclude that well-developed collateral vessels to a complete occluded artery prevent severe asynergy at rest but not during stress.     

Correlation between myocardial structure and diastolic properties of the heart in chronic aortic valve disease: Effects of corrective surgery

Left ventricular end-diastolic properties were evaluated with cineangiography and pressure measurements before and 6 months after aortic valve replacement with a Björk-Shiley prosthesis in 10 patients with aortic stenosis, 7 patients with mixed aortic valve disease and 7 patients with aortic insufficiency. Mean left atrial pressure, left ventricular end-diastolic pressure, volume and wall thickness were measured, and the stiffness constant K_A and the elastic stiffness E_m were calculated. Myocardial cell diameter and the degree of myocardial fibrosis were determined with morphometric analysis of transmural needle biopsy specimens obtained from the left ventricular free wall at operation. Significant correlations were found between myocardial cell diameter and end-diastolic pressure (r = 0.63), mean left atrial pressure (r = 0.58), end-diastolic wall thickness (r = 0.80), K_A (r = 0.56) and E_m (r = 0.53). However, no significant correlation existed between percent fibrosis and any of these measurements. Before operation, end-diastolic left ventricular pressure, mean left atrial pressure, K_A and E_mwere significantly elevated in aortic stenosis and mixed aortic valve disease but not in aortic insufficiency. After valve replacement clinical improvement was seen in all patients. End-diastolic left ventricular pressure, mean left atrial pressure, enddiastolic volume and E_m decreased and normalized completely in all groups. End-diastolic wall thickness and K_A decreased significantly in aortic stenosis and mixed aortic valve disease (not in aortic insufficiency) but remained moderately elevated. Close correlations were found between end-diastolic wall thickness and K_A (r = 0.78) and between mean left atrial pressure and E_m (r = 0.85).

These results suggest (1) myocardial cell diameter, but not myocardial fibrosis, is a major determinant of end-diastolic properties of the left ventricle in chronic aortic valve disease. (2) Corrective surgery with a Björk-Shiley valve causes normalization of elastic stiffness of the chamber and of mean left atrial pressure, thus explaining the alleviation of congestive symptoms.     

Diagnosis of dissecting aortic aneurysm with suprasternal echocardiography

A 33 year old woman with Marfan's syndrome and aortic root dissection was studied with precordial and suprasternal echocardiography. The precordial approach revealed some typical features of aortic root dissection. With suprasternal echocardiography it was possible to visualize the characteristic diagnostic feature of this disease: within the aortic lumen an m-shaped pattern--the aortic intimal flap--moving downward to the posterior aortic wall during systole. The diagnosis was confirmed with aortic cineangiography and intraoperative findings. Thus, suprasternal echocardiography can be a useful method of detecting aortic root dissection, especially in patients with aortic arch dissection alone.     

Paroxysmal nonreentrant tachycardias due to simultaneous conduction in dual atrioventricular nodal pathways.

Electrophysiologic studies were performed in a 41 year old man for analysis of paroxysmal tachycardias appearing in various electrocardiographic patterns of supraventricular and ventricular bigeminy, junctional and ventricular tachycardia and atrial fibrillation, among others. All these arrhythmias were due to dual atrioventricular (A-V) nodal pathways with simultaneous dual fast and slow conduction of single atrial beats at a normal basic sinus rate. Moderate changes in sinus rate and in fast or slow pathway conduction times, or both, changed the position of the slowly conducted beats between the neighboring two fast conducted beats and resulted in various electrocardiographic manifestations of the conduction disturbance. Different blocks, such as second degree type 1, 2:1, 3:1 and possibly also type II, in one of the two pathways and occasionally aberrant conduction induced even more unusual tracings. After intravenous injection of 25 mg of ajmaline, unexpected lengthening and shortening of the A-H interval occurred, suggesting variable shifts between fast and slow pathway conduction. The incidence of dual A-V nodal pathways is discussed; it was documented in 17 (4.2 percent) of 405 patients studied. A theoretical model of A-V nodal conduction is proposed to explain its normal properties and abnormal patterns.     

Prevalence of aortic valve prolapse with bicuspid aortic valve and its relation to aortic regurgitation: a cross-sectional echocardiographic study

Although aortic valve prolapse (AVP) has been suggested as a cause of aortic regurgitation (AR) in patients with bicuspid aortic valves, neither the frequency of AVP nor its relation to AR in this setting has been defined. To assess these relations, 64 patients with bicuspid aortic valves diagnosed by 2-dimensional echocardiography and 20 normal subjects, similarly distributed according to age and sex, were studied. The presence and degree of AVP were defined using 3 quantitative terms: aortic valve prolapse distance (AVPD), area (AVPA) and volume (AVPV). Each was corrected (c) for patient size with reference to the diameter of the aorta at the level of insertion of the valve cusps. In normal subjects, the AVPDc averaged 0.09 +/- 0.06 (range 0 to 0.16) and the AVPAc averaged 0.08 +/- 0.06 cm (range 0 to 0.15). In patients with bicuspid aortic valves, the AVPDc averaged 0.26 +/- 0.10 (range 0.11 to 0.59, p = 0.00005 vs normal subjects), whereas the AVPAc averaged 0.35 +/- 0.17 cm (range 0.05 to 0.90, p = 0.00005 vs normal subjects). When the AVPDc criteria were used, 81% of the bicuspid valves were abnormal; when the AVPAc criteria were used, 87% were abnormal. The degree of prolapse defined by the AVPVc, which considers both cusp area and degree of apical displacement, was significantly greater for patients with bicuspid aortic valve with clinical AR than for those without (p = 0.008). However, because of the overlap between groups, there was no point at which this measure uniquely separated patients with and without AR.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular arrhythmias before and late after aortic valve replacement

The influence of aortic valve replacement on the incidence of ventricular arrhythmias was studied by 24-hour Holter electrocardiographic monitoring in 45 patients immediately before and 14 ± 7 months after operation. Ventricular arrhythmias were graded according to the Lown criteria. Preoperative left ventricular (LV) ejection fraction (EF) was determined by angiography and postoperative LVEF by gated blood pool scintigraphy. Repetitive ventricular arrhythmias (Lown grade 4A/B) were associated with a reduced LVEF (< 55%) before and after operation. In 24 patients with preoperative normal LVEF (>- 55%) (group A), mean LVEF remained unchanged after operation (72% vs 71 %). Pre- and postoperative ventricular premature complex (VPC) frequency (45 ± 99 vs 39 ± 94 VPC/24 hours and grade (1.3 vs 1.4) were not significantly different. However, in 17 patients with preoperative impaired LVEF (< 55%) (group B, LVEF preoperatively 40 ± 8%) and marked postoperative improvement (> 10%) (LVEF postoperatively 64 ± 7%), mean VPC frequency decreased from 536 to 69 VPCs/24 hours and mean VPC grade was reduced from 3.8 to 1.5. Complex VPCs were found preoperatively in all 17 patients of group B, but in only 5 patients after operation. Four patients had a reduced LVEF preoperatively and it did not improve postoperatively (group C). Postoperative Holter monitoring detected ventricular tachycardia in all 4 patients.This study indicates that repetitive VPCs are infrequent in patients with normal LVEF before and late after aortic valve replacement. In patients with impaired LVEF and complex VPCs preoperatively, the postoperative improvement of LV function is usually accompanied by a reduction of frequent and complex VPCs.     

Ventricular arrhythmias late after aortic valve replacement and their relation to left ventricular performance

Sudden unexplained death is a common cause of late mortality after aortic valve replacement. To evaluate the occurrence of ventricular arrhythmia in patients with aortic valve replacement, two 24 hour ambulatory electrocardiographic recordings were obtained in 45 such patients (mean age 55 years) who had undergone replacement an average of 3.3 years previously. In 43 patients, ventricular arrhythmia was detected; it was rare (mean premature ventricular complex frequency less than $\text{1}\text{15}$ min) in 18 patients (40 percent), moderately frequent (mean frequency $\text{1?}\text{10}\text{15}$ min) in 14 patients (31 percent) and frequent (mean frequency more than $\text{10}\text{15}$ min) in 11 patients (24 percent). Multiformity was noted in 40 (89 percent), bigeminy in 27 (60 percent), couplets in 27 (60 percent) and ventricular tachycardia in 16 (36 percent) of the 45 patients studied. The occurrence of ventricular arrhythmia was not related to the predominant hemodynamic lesion or to the presence of coronary artery disease as determined at the time of preoperative cardiac catheterization. Radionuclide left ventricular ejection fraction, determined at the time of electrocardiographic monitoring in 39 patients, demonstrated normal left ventricular function (ejection fraction greater than 50 percent) in 27 patients (60 percent), moderately depressed function (ejection fraction 36 to 50 percent) in 8 (21 percent) and severe dysfunction in 4 (10 percent). When patients with abnormal versus normal left ventricular performance were compared, the mean premature ventricular complex frequency was $\text{21 ±}\text{26}\text{15}\text{min}\text{versus}\text{5 ±}\text{11}\text{15}\text{min (}\text{p}\text{< 0.01)}$; couplets occurred in 10 (83 percent) of 12 versus 13 (48 percent) of 27 patients (p < 0.05) and ventricular tachycardia in 8 (75 percent) of 12 versus 6 (22 percent) of 27 patients (p < 0.01). Patients exhibiting ventricular tachycardia had a mean left ventricular ejection fraction of 47 ± 14 percent compared with 62 ± 13 percent in patients without this arrhythmia (p < 0.005). This study indicates that significant ventricular arrhythmias, including ventricular tachycardia, are common late after aortic valve replacement. In addition, a relation exists between occurrence of arrhythmia and left ventricular function abnormalities.     

Prediction of postoperative performance in aortic valve disease

A new direct method has been developed for predicting postoperative performance in patients undergoing aortic valve replacement. Employing micromanometry and cineangiography, a number of conventional hemodynamic and angiographic variables, including the peak value of the first derivative of ventricular pressure divided by ventricular pressure (dP/dt/P)_max were evaluated in 171 patients studied preoperatively and in 44 patients studied pre- and postoperatively with an additional 14 patients serving as control subjects. Normal contractile state relations (dP/dt/P)_max versus end-diastolic pressure (over a range of 15 mm Hg or less to more than 15 mm Hg) were derived from patients whose preoperative ejection fraction and peak wall'stress were equal to or more than control mean — 2 standard deviations. Postoperative function was predicted to be abnormal (ejection fraction less than control mean — 2 standard deviations) if preoperative values of (dP/dt/P)_max and enddiastolic pressure fell below the 95 percent confidence bands of these contractile state relations.The method accurately predicted postoperative function in 40 of 44 patients with a sensitivity of 100 percent. This result was confirmed by a discriminant function analysis (based on preoperative ejection fraction, end-diastolic pressure and [dP/dt/P]_max) that yielded correct classifications in 42 of 44 patients. These studies indicate that the preoperative contractile state of the myocardium is the major determinant of postoperative performance in aortic valve disease.     

Ventricular arrhythmias in aortic valve disease: Analysis of 102 patients

Frequency and grade of ventricular arrhythmias in patients with isolated aortic stenosis (AS) or regurgitation (AR) were determined by 24-hour ambulatory electrocardiographic monitoring. The occurrence of ventricular arrhythmias in patients with aortic valve disease was compared with that in matched control subjects without aortic valve disease. Complex arrhythmias were significantly more prevalent in patients with valve disease than in control subjects (40 of 102 vs 19 of 102); the significant difference occurred in patients without concomitant coronary artery disease (CAD). In patients with valve disease without CAD, complex arrhythmias were significantly more common than in normal control subjects (22 of 65 vs 4 of 64); in the presence of CAD, complex arrhythmias were as prevalent in those with aortic valve disease as in those without it (18 of 37 vs 15 of 37, respectively). Among patients with AS or AR, arrhythmia occurrence and grade of ventricular ectopic activity were not related to the degree of AS or AR, ventricular hemodynamics or the presence or absence of concomitant CAD.     

Myocardial oxygen consumption in chronic heart disease: role of wall stress, hypertrophy and coronary reserve.

The relations between left ventricular mass, mass to volume ratio, systolic wall stress and myocardial oxygen consumption were analyzed in 187 patients with chronic heart disease. The degree of left ventricular hypertrophy is determined by mass, the mass to volume ratio, and pressure and, hence, systolic wall stress. For each condition an inverse relation exists between mass to volume ratio and peak systolic wall stress. In chronic heart disease at least two types of inappropriate left ventricular hypertrophy may occur: (1) low stress hypertrophy with an increased mass to volume ratio, normal left ventricular function and normal or reduced oxygen consumption (MVO₂), whereas (2) high stress hypertrophy has a normal or low mass to volume ratio, impaired left ventricular function and an increased MVO₂. The range of systolic wall stress was 100 to 450 × 10³, dynes/cm² and reflects the stress that could be altered by inotropic interventions and changes in systolic pressure. A similar reserve capacity is present for both the metabolic and the coronary reserves. Total left ventricular oxygen consumption is related to total left ventricular mass. This relation is influenced by the degree of viability of left ventricular mass, by the mass to volume ratio and by inotropic interventions. Left ventricular oxygen consumption per viable mass unit (MVO₂) is significantly correlated with the systolic force per unit cross-sectional area of the left ventricular wall, that is, to left ventricular systolic wall stress.It is concluded that peak systolic wall stress represents one of the major determinants of myocardial oxygen consumption and of ventricular performance. It closely relates to the appropriateness of left ventricular hypertrophy, which may be defined by the relation between systolic pressure, mass to volume ratio and peak systolic wall stress.