Absence of gender differences in clinical outcomes in patients with cardiogenic shock complicating acute myocardial infarction. A report from the SHOCK Trial Registry.

OBJECTIVES: The aim of this study was to assess the impact of gender on clinical course and in-hospital mortality in patients with cardiogenic shock (CS) complicating acute myocardial infarction (AMI). BACKGROUND: Previous studies have demonstrated higher mortality for women compared with men with ST elevation myocardial infarctions and higher rates of CS after AMI. The influence of gender and its interaction with various treatment strategies on clinical outcomes once CS develops is unclear. METHODS: Using the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? (SHOCK) Registry database of 1,190 patients with suspected CS in the setting of AMI, we examined shock etiologies by gender. Among the 884 patients with predominant left ventricular (LV) failure, we compared the patient demographics, angiographic and hemodynamic findings, treatment approaches as well as the clinical outcomes of women versus men. This study had a 97% power to detect a 10% absolute difference in mortality by gender. RESULTS: Left ventricular failure was the most frequent cause of CS for both gender groups. Women in the SHOCK Registry had a significantly higher incidence of mechanical complications including ventricular septal rupture and acute severe mitral regurgitation. Among patients with predominant LV failure, women were, on average, 4.6 years older, had a higher incidence of hypertension, diabetes and a lower cardiac index. The overall mortality rate for the entire cohort was high (61%). After adjustment for differences in patient demographics and treatment approaches, there was no significant difference in in-hospital mortality between the two gender groups (odds ratio = 1.03, 95% confidence interval of 0.73 to 1.43, p = 0.88). Mortality was also similar for women and men who were selected for revascularization (44% vs. 38%, p = 0.244). CONCLUSIONS: Women with CS complicating AMI had more frequent adverse clinical characteristics and mechanical complications. Women derived the same benefit as men from revascularization, and gender was not independently associated with in-hospital mortality in the SHOCK Registry.

A randomized trial of stenting with or without balloon predilation for the treatment of coronary artery disease.

BACKGROUND: Stent placement has historically been preceded by predilation of the target lesion with percutaneous transluminal coronary angioplasty. Direct stent implantation, without predilation, has the potential to have a favorable impact on procedure cost by reducing the number of devices used, contrast administered, and procedure time. METHODS AND RESULTS: We conducted a prospective randomized trial to compare the economic outcome of stenting with or without predilation. Inclusion criteria included intention to treat a single lesion with a coronary stent in a vessel with a reference diameter >2.4 mm. Exclusion criteria included total occlusions, culprit lesion within a saphenous vein graft, lesion length >25 mm, patients within 48 hours of an acute myocardial infarction, and patients unable to be treated with aspirin and clopidogrel. From September 1999 to March 2000, 77 patients were randomized to direct stent implantation (n = 37) or balloon-facilitated stenting (n = 40). Stent placement was successful in all patients. Crossover to predilation was required in 2 patients in the direct stent group because of inability to deliver the stent. Compared with balloon-facilitated stenting, direct stenting used fewer catheter devices (1.4 +/- 0.7 vs 2.5 +/- 0.8, P <.001), less contrast (92.7 +/- 43.1 mL vs 117.4 +/- 61.0 mL, P =.04), and less fluoroscopy time (7.5 +/- 3.9 minutes vs 11.6 +/- 8.3 minutes, P =.006). No difference in procedural complications or predischarge outcome was found. No difference in major adverse cardiovascular events was found at 6-month follow-up. CONCLUSION: Direct stenting is a safe and successful procedure that reduces the number of devices used, fluoroscopy time, and contrast administration.

Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK?

OBJECTIVES: We wished to assess the profile and outcomes of patients with ventricular septal rupture (VSR) in the setting of cardiogenic shock (CS) complicating acute myocardial infarction (MI). BACKGROUND: Cardiogenic shock is often seen with VSR complicating acute MI. Despite surgical therapy, mortality in such patients is high. METHODS: We analyzed 939 patients enrolled in the SHOCK Trial Registry of CS in acute infarction, comparing 55 patients whose shock was associated with VSR with 884 patients who had predominant left ventricular failure. RESULTS: Rupture occurred a median 16 h after infarction. Patients with VSR tended to be older (p = 0.053), were more often female (p = 0.002) and less often had previous infarction (p < 0.001), diabetes mellitus (p = 0.015) or smoking history (p = 0.033). They also underwent right-heart catheterization, intra-aortic balloon pumping and bypass surgery significantly more often. Although patients with rupture had less severe coronary disease, their in-hospital mortality was higher (87% vs. 61%, p < 0.001). Surgical repair was performed in 31 patients with rupture (21 had concomitant bypass surgery); 6 (19%) survived. Of the 24 patients managed medically, only 1 survived. CONCLUSIONS: There is a high in-hospital mortality rate when CS develops as a result of VSR. Ventricular septal rupture may occur early after infarction, and women and the elderly may be more susceptible. Although the prognosis is poor, surgery remains the best therapeutic option in this setting.

Clinical and nonclinical correlates of racial and ethnic differences in recommendation patterns for coronary revascularization.

BACKGROUND: We sought to determine whether gender or racial differences exist in recommendations for coronary revascularization in a multiracial patient population undergoing their first coronary angiography at an academic institution from 1990-1993 for the evaluation of coronary artery disease (CAD). HYPOTHESIS: For patients with clinically significant CAD, no racial differences exist in the recommendation to revascularization following coronary angiography. METHODS: The main outcome measure was a recommendation for coronary revascularization such as percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass graft (CABG) for patients with clinically significant CAD (n = 590). The primary multiple logistic regression analysis focused on only those patients with angiographically severe disease, defined as triple-vessel or left main CAD (n = 180). Race was trichotomized into Hispanic, black, and white to ascertain whether any differential effects of race/ethnicity existed while controlling for age, gender, ejection fraction, angina, diabetes, hypertension, and peripheral vascular disease. A medical record review for all patients with severe CAD, who were given a recommendation for medical therapy, was conducted to ascertain whether previously unmeasured clinical factors or nonclinical factors may have precluded a PTCA/CABG recommendation. RESULTS: Hispanics with severe disease were significantly less likely than whites to be given a recommendation for PTCA/CABG following angiography [odds ratio (OR) = 0.39; 95% confidence interval (CI) (0.17, 0.92)]. Blacks were 67% as likely as whites to be given such a recommendation [OR = 0.67; 95% CI (0.17, 2.71)]. Medical records, reviewed for 35 of 40 of these patients given a recommendation for medical therapy, revealed that 6 patients eventually had PTCA/CABG within 6 months due to precipitating ischemic events; 9 had such severe or diffuse disease that revascularization did not appear to be an alternative, and 2 patients opted for medical therapy. CONCLUSIONS: Racial differences were manifested in the recommendations made following angiography and may be explained by previously unmeasured clinical as well as nonclinical factors.

Role of low-molecular-weight heparins in the management of patients with unstable angina pectoris and non-Q-wave acute myocardial infarction.

The development of effective approaches to the management of the unstable coronary syndromes has resulted from an improved understanding of interactions between the vascular wall, platelets, and coagulation factors, and of their response to pharmacologic and mechanical interventions. Furthermore, the occurrence of frequent adverse events after discharge in patients with unstable coronary artery disease (CAD) treated with these therapies alone would argue that, for many of these patients, such stabilization is not the end of the therapeutic pathway; rather, these therapies are for many a preparation for ultimate revascularization, to preserve myocardium and minimize periprocedural complications. The low-molecular-weight heparins with their unique pharmacology offer a new option in the therapy of patients with unstable CAD. There is now extensive experience in the use of several of the low-molecular-weight heparins, particularly dalteparin and enoxaparin, in the management of patients with unstable angina. Several trials have investigated the questions raised by these observations, taking advantage of the unique pharmacologic properties of the low-molecular-weight heparins for both acute inpatient use and prolonged outpatient administration. Although differences in study design preclude direct comparison between the available low-molecular-weight heparins, in these trials low-molecular-weight heparins have been shown to be effective alternatives to conventional heparin for the management of patients with unstable angina and non-Q-wave infarction. These include several small-scale trials and the larger FRagmin during InStability in Coronary artery disease (FRISC), Fragmin in Unstable Coronary Artery Disease (FRIC), Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q-Wave Coronary Events (ESSENCE), FRISC II, and Thrombolysis in Myocardial Infarction (TIMI)-11B trials. Thus, the low-molecular-weight heparins appear to be a superior alternative to traditionally administered intravenous unfractionated heparin. They are more predictable in action, do not require frequent activated partial thromboplastin time (aPTT) measurements and dosage adjustments, are easier to administer, and are potentially more efficacious. With their proven efficacy, predictability of action, and convenience of administration and dosing, there are very good reasons for selecting them as first-line therapies for patients presenting with unstable angina and non-Q-wave myocardial infarction.

Time to dP/dt(max), a useful index for evaluation of contractility in the catheterization laboratory.

HYPOTHESIS: The time from onset of contraction to dP/dt(max), td, is suggested as an index of contractility in the catheterization laboratory. METHODS: We studied 22 normal patients and 18 patients with myocardial failure in the catheterization laboratory. The two groups were completely separated on the td-heart rate (HR) plane. In the normal patients, HR = 73 +/- 19 beats/min, td = 73 +/- 11 ms, and an inverse linear relation td = 109-0.49 x HR (p < 0.001) exist. In the patients with myocardial failure, despite significantly higher HR than in normal patients (HR = 93 +/- 14 beats/min) (p < 0.001), td paradoxically increased (td = 89 +/- 11 ms, p < 0.0001). CONCLUSIONS: These findings support a mathematical analysis of the left ventricular pressure (LVP) during isovolumic contraction in the time domain which shows that td and (dP/dt)/P reflect the time-dependent aspects of contraction and, hence, decrease with increasing contractility. This study shows that td, at any given HR, is a reliable index of contractility. Thus, a ready-to-use td-HR plot containing a well-based separation line can provide a reliable and simple method for determining contractility in the catheterization laboratory by examining whether a patient's td value at any HR is below (normal) or above (impaired contractility) the separation line.

Normalization of diastolic dysfunction in aortic stenosis late after valve replacement.

BACKGROUND: The remodeling of the left ventricle in patients with aortic stenosis after aortic valve replacement (AVR) is a complex process involving structural and functional changes. METHODS AND RESULTS: Twenty-two patients were included in the present analysis. Twelve patients with severe aortic stenosis were studied before surgery, early (22 +/- 8 months) and late (81 +/- 22 months) after AVR using left ventricular biplane angiograms, high-fidelity pressure measurements, and endomyocardial biopsies. Ten healthy subjects were used as controls. Left ventricular systolic function was assessed from biplane ejection fraction; and diastolic function from the time constant of relaxation, the peak filling rate, and the myocardial stiffness constant. Left ventricular structure was evaluated from interstitial fibrosis, fibrous content, and muscle fiber diameter. Left ventricular muscle mass was significantly increased before surgery in patients with aortic stenosis and remained increased early after surgery, although there was a 35% decrease. Late after AVR, muscle mass decreased significantly but remained slightly (P = NS) elevated. Left ventricular ejection fraction increased slightly after AVR. Left ventricular relaxation was significantly prolonged before surgery and returned toward normal early and late after AVR. Peak filling rates remained unchanged before and after surgery. Myocardial stiffness constant was increased before surgery in patients with aortic stenosis compared with controls and increased even further early after AVR but was normalized late after surgery. Muscle fiber diameter was elevated in patients with aortic stenosis before and after surgery compared with controls; however, it decreased significantly early and late after AVR with respect to preoperative data but remained hypertrophied even late after surgery. Interstitial fibrosis and fibrous contents were larger before surgery than in control subjects and increased even more early but decreased significantly late after AVR. CONCLUSIONS: Diastolic stiffness increases in aortic stenosis early after AVR parallel to the increase in interstitial fibrosis, whereas relaxation rate decreases with a reduction in left ventricular muscle mass. Late after AVR, both diastolic stiffness and relaxation are normalized due to the regression of both muscular and nonmuscular tissue. Thus, reversal of diastolic dysfunction in aortic stenosis takes years and is accompanied by a slow regression of interstitial fibrosis.

Regional specificity of peak hyperemic response in patients with congestive heart failure: correlation with peak aerobic capacity.

OBJECTIVES: The aim of this study was to compare peak reactive hyperemic blood flows in the forearm and calf of patients with congestive heart failure and in age- and gender-matched normal subjects. In addition, we attempted to correlate peak oxygen consumption with forearm and calf peak reactive hyperemic flows in the patients with heart failure. BACKGROUND: Disparate results have been reported regarding forearm peak reactive hyperemia in patients with congestive heart failure. Because training significantly increases peak reactive hyperemic flow in normal subjects, we hypothesized that in patients with congestive heart failure who curtail walking because of exertional symptoms, calf peak reactive hyperemic flow would be preferentially attenuated and that impairment of calf vasculature may correlate with peak oxygen consumption. METHODS: Forearm and calf blood flows were measured by venous occlusive plethysmography at rest and after 5 min of arterial occlusion in 46 patients with congestive heart failure and 7 age- and gender-matched normal subjects. Peak oxygen consumption was measured during graded exercise on a bicycle ergometer. RESULTS: Calf peak reactive hyperemic flow was lower in patients with congestive heart failure than in normal subjects (22 +/- 1 vs. 32.5 +/- 3.5 ml/min per 100 ml, p < 0.001), whereas forearm peak reactive hyperemic flows were similar in the two groups. Calf peak reactive hyperemic flow was linearly related to peak oxygen consumption (r = 0.58, p < 0.0001), but forearm peak reactive hyperemic flow was not. Forearm and calf peak reactive hyperemic flows were not related at rest or after 5 min of arterial occlusion in the patients with heart failure. CONCLUSIONS: Calf peak reactive hyperemic flow is reduced in patients with congestive heart failure, whereas forearm peak reactive hyperemic flow is identical to that of age- and gender-matched normal subjects. Calf peak reactive hyperemic flow is linearly related to peak oxygen consumption in patients with congestive heart failure, but forearm peak reactive hyperemic flow is not.

Thrombolysis: the need for a critical review.

The (Thrombolysis in Myocardial Infarction) TIMI-I trial led to the hypothesis that the greater reperfusion rate seen with recombinant tissue-type plasminogen activator (rt-PA) versus streptokinase would result in greater reductions in infarct size and mortality in patients with acute myocardial infarction. Despite extensive investigation, no trial comparing rt-PA with streptokinase (European Cooperative Study Group, Plasminogen Activator Italian Multicenter Study [PAIMS], Gruppo Italiano per lo Studio della Sopravvivenze nell'Infarto Miocardico [GISSI-2], International Study on Infarct Survival [ISIS-3], even TIMI-I itself) nor rt-PA and anisoylated plasminogen-streptokinase activator complex (APSAC or anistreplase) (Bassand, TEAM-3, ISIS-3), have confirmed this hypothesis. In a reversal of traditional scientific method, the studies, rather than the unconfirmed hypothesis, have been rejected. A lack of independent review of this subject may have contributed to this outcome. It is proposed that standards of review and editorial comment mandating true critical distance and independence be followed, permitting greater independence of scientific inquiry, review and debate.

Left ventricular passive diastolic properties in chronic mitral regurgitation.

BACKGROUND: In chronic mitral regurgitation, the myocardium responds to the increased filling volume by geometric alteration and eccentric hypertrophy. This study was designed to evaluate the effects of a pure volume overload on left ventricular diastolic chamber and myocardial properties and to assess the relation of passive diastolic function to systolic ejection performance. METHODS AND RESULTS: By use of simultaneous cineangiography and left ventricular micromanometry, left ventricular passive diastolic stiffness was evaluated in nine normal controls (group 1), 14 patients with chronic mitral regurgitation and a normal ejection fraction (greater than or equal to 57%, group 2), and 13 patients with mitral regurgitation and a reduced ejection fraction (less than 57%, group 3). Passive diastolic function was evaluated by using a three-constant elastic model. Left ventricular chamber properties were represented by the relation of pressure to volume; myocardial properties were evaluated by relating myocardial midwall stress to midwall strain. The constant of left ventricular chamber stiffness was decreased in group 2 compared with controls (p less than 0.05) but it was normal in group 3. The constant of myocardial stiffness was increased in group 3 compared with groups 1 and 2 (p less than 0.01). Among patients with mitral regurgitation, there was a significant inverse relation between ejection fraction and the constant of myocardial stiffness (r = -0.83). CONCLUSIONS: The chronic adaptation to volume overload in chronic mitral regurgitation tends to decrease left ventricular chamber stiffness. Patients with mitral regurgitation and a depressed ejection fraction demonstrated diastolic myocardial dysfunction. Compromised diastolic function in patients with chronic mitral regurgitation and reduced systolic performance may contribute to the clinical manifestations of congestive heart failure.

Flosequinan: a vasodilator with positive inotropic activity.

Flosequinan is an oral arterial and venous vasodilator that is currently under investigation for the treatment of congestive heart failure. The effects of flosequinan on ventricular performance and myocardial contractility were studied in 10 patients with severe congestive heart failure during right and left cardiac catheterization. Sixty minutes after a 100 mg oral dose of flosequinan, the peak rate of rise in left ventricular pressure (dP/dt) increased from 940 +/- 180 to 1050 +/- 240 mm Hg/sec (p less than 0.05), while left ventricular end-diastolic pressure decreased from 32 +/- 5 to 26 +/- 8 mm Hg (p less than 0.05), and cardiac index increased (2.1 +/- 0.4 to 2.3 +/- 0.5 L/min/m2, (p less than 0.05). The mean pulmonary artery pressure and vascular resistance decreased from 40 +/- 8 to 33 +/- 12 mm Hg (p less than 0.05) and from 330 +/- 240 to 290 +/- 170 dyne-sec/cm5 (p less than 0.05), respectively. Heart rate, mean aortic pressure, right atrial pressure, systemic vascular resistance, and serum norepinephrine levels did not change significantly. The increase in left ventricular peak dP/dt that was concomitant with a decrease in left ventricular end-diastolic pressure, and no change in systemic arterial pressure or sympathetic tone, argue for a direct positive inotropic effect of flosequinan.

Function and structure of the failing left ventricular myocardium in aortic valve disease before and after valve replacement.

Left ventricular (LV) cineangiography and endomyocardial biopsies were performed preoperatively in 49 patients (pts) with aortic stenosis (AS) and 35 pts with aortic insufficiency (AI). LV failure (group 1) was present in 15 pts with AS and 17 pts with AI. In these pts ejection fraction (EF) was less than 57% and either cardiac index was less than 2.5 L/min/m2 and/or LV end-diastolic pressure was greater than 20 mm Hg. Macroscopic LV hypertrophy was assessed by angiographic muscle mass (LMMI, g/m2). Morphometric evaluation of LV biopsies included the determination of muscle fiber diameter (MFD, mu), percent interstitial fibrosis (IF, %), volume fraction of myofibrils (VFM, %) and the calculation of LV fibrous content (FC, g/m2). Pts of group 1 and 2 were restudied 22.5 and 24.0 months, respectively, after successful aortic valve replacement. Preoperatively, group 1 pts had a significantly higher LMMI, MFD, and FC than did the patients in group 2 (non-failing group consisting of 34 pts with AS and 18 with AI). IF and VFM did not differ. After surgery EF increased significantly from 44% to 59% in group 1, whereas it remained unchanged in group 2 (66%). Although in both groups LMMI and MFD decreased significantly these quantities were increased after surgery in group 1 as compared to group 2. IF, VFM, and FC did not change significantly in group 1 after valve replacement. There was no difference in these latter three quantities between groups 1 and 2 after surgery. It is concluded that 1) macroscopic and microscopic hypertrophy is more marked in the failing than in the non-failing left ventricle, 2) left ventricular pump function is not related to percent interstitial fibrosis, and 3) at an intermediate time after aortic valve replacement pts with previously failing left ventricle show considerable improvement of ejection performance, but residual hypertrophy persists.

Effect of a modified, well-tolerated niacin regimen on serum total cholesterol, high density lipoprotein cholesterol and the cholesterol to high density lipoprotein ratio.

One hundred one patients with coronary artery disease and pretreatment ratios of total cholesterol to high density lipoprotein (HDL) cholesterol greater than 4.0 were treated with niacin, commencing at low dosages (100 to 250 mg twice daily) and gradually increasing the dosage over 4 to 8 weeks to 1,000 mg twice daily. Dosage adjustments were made to minimize side effects. At a mean follow-up duration of 11 +/- 7 months, and a mean dosage of 1,415 +/- 698 mg/day, the group had a 13% reduction in total cholesterol, 31% increase in HDL and 32% decrease in the cholesterol to HDL ratio. A subgroup of 62 patients taking greater than 1,000 mg/day of niacin had an 18% reduction in total cholesterol, 32% increase in HDL and 36% improvement in the cholesterol to HDL ratio. A subgroup of 39 patients taking less than or equal to 1,000 mg/day of niacin had only a 5% reduction in total cholesterol, although a 29% increase in HDL and a 24% decrease in the cholesterol to HDL ratio were recorded. Side effects of niacin were reported in 38% of the patients, but led to discontinuation of therapy in only 4. Niacin can be administered in a fashion that is well tolerated, inexpensive and very effective in improving the cholesterol to HDL ratio.

Left ventricular myocardial structure in aortic valve disease before, intermediate, and late after aortic valve replacement.

Left ventricular biplane cineangiography, micromanometry, and endomyocardial biopsies were performed in 27 patients with aortic stenosis (AS) and in 17 patients with aortic insufficiency (AI). Twenty-three patients with AS and 15 with AI were restudied at an intermediate time (18 months after successful valve replacement), and nine patients with AS and six with AI were restudied late (70 and 62 months after surgery). Biopsy samples were evaluated for muscle fiber diameter, percent interstitial fibrosis, and volume fraction of myofibrils. In control biopsy samples obtained from five donor hearts at transplantation, these morphometric variables averaged 21.2 microns, 7.0%, and 57.2%, respectively. After surgery, mass determined by cineangiography decreased from 186 to 115 and 94 g/m2 in patients with AS and from 201 to 131 and 93 g/m2 in patients with AI. At the three studies, muscle fiber diameter was 30.9, 28.0, and 28.7 microns in patients with AS and was 31.4, 27.6, and 26.4 microns in patients with AI. Percent interstitial fibrosis was 18.2, 25.8, and 13.7% in patients with AS and was 20.4, 23.7, and 19.2% in patients with AI. Left ventricular fibrous content decreased from 34.2 to 29.8 and to 12.7 g/m2 in patients with AS and from 42.1 to 28.9 and to 18.9 g/m2 in patients with AI. Volume fraction of myofibrils was 57.7, 56.8, and 49.0% in patients with AS and was 56.8, 56.6 and 48.8% in patients with AI. Thus, the decrease of muscle mass determined by cineangiography at the intermediate time after valve replacement is mediated by regression of myocardial cellular hypertrophy in patients with AS and AI and in addition by a decrease of fibrous content in patients with AI. Late after surgery, left ventricular fibrous content also decreases in patients with AS. This late decrease associated with minor changes of end-diastolic volume may be important for improvement of increased diastolic myocardial stiffness. Even 6-7 years after valve replacement, incomplete regression of structural abnormalities of left ventricular hypertrophy still exists compared with the normal myocardium. The residually increased relative interstitial fibrosis and the small late postoperative decrease of volume fraction of myofibrils, associated with a prosthesis-related slight left ventricular pressure increase, are at the origin of a persistent systolic overload at the myofibrillar level.

Left ventricular volume determination in dogs: a comparison between conductance technique and angiocardiography.

Left ventricular (LV) volume was determined simultaneously by monoplane cineangiocardiography and conductivity using a multielectrode conductance catheter at rest and during pressure loading in seven mongrel dogs (mean body weight 22 kg). LV volumes were calculated frame-by-frame (75 frames s-1) by angiocardiography and matched with instantaneous volumes obtained by conductivity. There was an excellent correlation between the two techniques at rest (correlation coefficient, r = 0.96) and during pressure loading (r = 0.92) when the data of each dog were pooled. The standard error of estimate of the mean angiographic volume was 4%. The slope of the regression analysis showed a small but significant (P less than 0.01) decrease from 0.365 at rest to 0.289 during pressure loading, whereas the intercept remained unchanged (24 versus 26 ml). Since no calibration for parallel conductivity of the surrounding tissue was performed, LV end-systolic volume was significantly over- and LV ejection fraction significantly underestimated whereas LV end-diastolic volume was estimated correctly by the conductance technique. It is concluded that LV end-diastolic volume can be determined accurately by the conductance technique in dogs. However, LV end-systolic volume is significantly over- and ejection fraction significantly underestimated. Since there is a good correlation between angiocardiography and conductivity, exact determination of LV volumes and ejection fraction is feasible using a correction factor. The change in slope of the regression equation between angiocardiography and conductivity suggests a change in conductivity of the surrounding tissue during pressure loading which limits the application of the conductance catheter to stable haemodynamic situations or calls for repeated calibrations by an independent technique during acute interventions.

Time course of regression of left ventricular hypertrophy after aortic valve replacement.

To assess the time course and extent of regression of myocardial hypertrophy after removal of the inciting hemodynamic stress, 21 patients with either aortic stenosis or aortic insufficiency were studied preoperatively, after an intermediate period (1.6 +/- 0.5 years), and late (8.1 +/- 2.9 years) after aortic valve replacement, and results were compared with those in 11 control patients. After aortic valve replacement there was significant hemodynamic improvement, with a fall in the left ventricular end-diastolic volume index (164 +/- 73 to 105 +/- 35 ml/m2, p less than .01), a fall in left heart filling pressure (19 +/- 9 to 12 +/- 5 mm Hg, p less than .01), and maintenance of the cardiac index (3.3 +/- 0.8 to 3.5 +/- 0.8 liters/min/m2, NS) and left ventricular ejection fraction (60 +/- 13% to 64 +/- 10%, NS). By the late study the cardiac index (4.0 +/- 0.6 liters/min/m2, p less than .01) and left ventricular ejection fraction (66 +/- 15%, p less than .05) had further increased and were significantly greater than before surgery. For the group as a whole, the left ventricular muscle mass index fell 31% after surgery by the time of the intermediate postoperative study (174 +/- 38 vs 120 +/- 29 g/m2, p less than .01), and a further 13% from the intermediate to the late study (105 +/- 32 g/m2, p less than .05). At the preoperative study left ventricular muscle mass index was greatest in those patients with aortic insufficiency (191 +/- 36 g/m2), and greater in those with aortic stenosis (158 +/- 33 g/m2) than in control subjects (85 +/- 9 g/m2, p less than .05). At the intermediate postoperative study left ventricular muscle mass index remained significantly higher in both those with preoperative aortic insufficiency (128 +/- 29 g/m2) and those with stenosis (114 +/- 27 g/m2) than in the control subjects (p less than .01). By the time of the late postoperative study there were no longer any significant differences in left ventricular muscle mass index. Thus, the regression of myocardial hypertrophy is a process that occurs over many years after correction of the primary hemodynamic abnormality. As this process of myocardial remodeling occurs, continued improvement in cardiac function may occur, and the improvement occurring between the intermediate and late postoperative studies at a slight but constant afterload excess (inherent in the relative stenosis of the aortic prosthesis) suggests that the hypertrophied myocardium is operating at a reduced level compared with normal myocardium.

Left ventricular systolic function in aortic stenosis.

In aortic valve stenosis, concentric hypertrophy develops which is characterized by a reduced end-diastolic radius-to-wall thickness ratio (r/h) with an essentially normal cavity shape. As long as the product of (r/h) and LV systolic pressure remains constant, hypertrophy is appropriate. An increase in the product, which represents an increase in wall stress signals inadequate LV hypertrophy. Although at first glance, massive LV hypertrophy appears favourable for the maintenance of a normal LV ejection fraction in aortic stenosis, data from 23 studies of the literature have shown an inverse relationship between ejection fraction and LV angiographic mass m-2 (r = -0.59). Both a degree of hypertrophy inadequate to keep systolic wall stress within normal limits and a reduction of LV contractility may explain the depression of ejection fraction when LV angiographic mass is sizeably increased. Conversely, a normal ejection fraction in aortic stenosis may not be indicative of normal systolic myocardial function under all circumstances. In the presence of mildly reduced contractility, a normal ejection fraction may be maintained by the use of preload reserve. Assessment of myocardial structure from LV endomyocardial biopsies revealed no differences in muscle fibre diameter, interstitial fibrosis and volume fraction of myofibrils between patients with aortic stenosis having a normal and those with a depressed ejection fraction. Preoperative ejection fraction is a poor predictor of postoperative survival, whereas markedly increased preoperative angiographic mass and end-systolic volume have been reported to predict an unsatisfactory postoperative outcome characterized by either death or poor LV function.

Abnormal exercise hemodynamics in patients with normal systolic function late after aortic valve replacement.

We studied the hemodynamic response to supine bicycle exercise in 20 patients late (10 +/- 2 years) after aortic valve replacement (for aortic stenosis in 12 patients, aortic insufficiency in six patients, and for combined stenosis and insufficiency in two patients). The pulmonary artery wedge pressure was obtained with a pulmonary artery balloon catheter, and left ventriculography was performed by digital-subtraction angiography after injection of radiographic contrast into the pulmonary artery. These patients were compared with 11 control subjects with no or minimal cardiac disease studied routinely for evaluation of chest pain in whom left ventricular end-diastolic pressure and a direct contrast ventriculogram were obtained. Compared with the control population, the study population had similar left heart filling pressures (7 +/- 3 vs 9 +/- 3 mm Hg, NS), but higher left ventricular ejection fractions (75 +/- 7% vs 67 +/- 7%, p less than .02) and higher left ventricular muscle mass indexes (106 +/- 28 vs 85 +/- 9 g/m2, p less than .01). Elevated myocardial muscle mass led to lower systolic wall stress in the study population than in the control subjects (254 +/- 65 vs 320 +/- 49 10(3).dynes/cm2, p less than .01) and might explain the higher ejection fraction observed. Fourteen patients had a normal response to exercise (with left heart filling pressures of 16 +/- 4 vs 18 +/- 2 mm Hg for control subjects, NS; and left ventricular ejection fraction of 77 +/- 8% vs 73 +/- 5% for control subjects, NS). However, while the remaining six patients had a normal exercise left ventricular ejection fraction (72 +/- 9%, NS), they had an abnormal rise in left heart filling pressure (33 +/- 8 mm Hg, p less than .01). Preoperatively these patients also had higher left ventricular mid- and end-diastolic pressures at similar diastolic volumes, suggesting a decrease in chamber compliance. Thus, late after aortic valve replacement there is a subgroup of patients who, despite normal hemodynamics and normal left ventricular systolic function as assessed by the left ventricular ejection fraction at rest, have an abnormal response to exercise characterized primarily by a substantial rise in left heart filling pressures. Preoperatively this group also has a decrease in diastolic chamber compliance despite nearly normal left ventricular ejection fractions. This abnormality appears to result from a primary derangement of diastolic function that is not evident at rest.

The relationship of afterload to ejection performance in chronic mitral regurgitation.

Simultaneous left ventricular micromanometry and biplane cineangiography were performed in nine control subjects (group 1), 14 patients with chronic mitral regurgitation and an ejection fraction of 57% or greater (group 2), and 13 patients with mitral regurgitation and an ejection fraction of less than 57% (group 3). End-diastolic volume index was increased in both groups with mitral regurgitation (p less than .001) compared with the control group. Left ventricular end-diastolic wall thickness did not differ among the three groups, but the left ventricular muscle mass index was greater in both groups with mitral regurgitation than in controls (p less than .001). End-diastolic pressure was elevated in both groups 2 and 3 compared with group 1 (p less than .05), but peak systolic, mean systolic, and incisural pressure were not different among the three groups. End-diastolic stress was larger in groups 2 and 3 than in group 1 (p less than .05). Muscle fiber stretch was greater in group 2 than in the control group (p less than .05) but was not different between the controls and group 3. End-systolic stress, determined as the circumferential stress at aortic valve closure, at the maximal pressure/volume ratio, or using a nonsimultaneous method, was larger in group 3 than in groups 1 and 2. Mean systolic stress was evaluated from aortic valve opening to aortic valve closure in all patients; mean stress from end-diastole to aortic valve closure and from end-diastole to minimum volume was assessed in mitral regurgitation alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of percutaneous transluminal coronary angioplasty for unstable angina pectoris after non-Q-wave acute myocardial infarction.

Without revascularization, patients with non-Q-wave acute myocardial infarction (AMI) are predisposed to angina, recurrent AMI and cardiac death. Percutaneous transluminal coronary angioplasty (PTCA) was performed in 68 patients with angina an average of 2.3 months after non-Q-wave AMI (41 anterior, 27 inferior). Mean diameter stenosis was 95%, with collateralized total occlusion of the infarct-related artery in 23 patients. PTCA was successful in 87% (59 of 68), with a mean residual stenosis of 30%. One patient had emergency bypass surgery. Long-term follow-up (average 17 +/- 10 months) was available for 58 of the 59 patients in whom PTCA was successful. Recurrent angina developed in 41% (24 of 58), but was relieved by repeat PTCA in 14, by late coronary artery bypass surgery in 4 and by medical therapy in 6. There was 1 nonfatal AMI, due to progressive disease in a nondilated vessel, and 1 noncardiac death At last follow-up, 46 of 58 patients (79%) were asymptomatic and fully active or employed. Thus, patients undergoing PTCA for angina after non-Q-wave AMI appear to have a relatively high clinical restenosis rate, but with repeat PTCA have a low incidence of subsequent angina, AMI and cardiac death.