bluuebunny/crossref_metadata_2025 huggingface dataset:
Sotalol in patients with Wolff-Parkinson-White syndrome.
Authors: Kunze K P , Schlüter M , Kuck K H
Published: June 2011

We evaluated the effects of intravenous and long-term oral sotalol treatment in 17 patients with an accessory atrioventricular (AV) pathway. All patients had a history of symptomatic supraventricular tachycardia. During electrophysiologic study intravenous (1.5 mg/kg body weight) and oral (240 to 320 mg/day) sotalol caused significant increases of sinus cycle length, AV nodal conduction time, and refractory periods of atrial and ventricular myocardium and accessory pathway. AV reciprocating tachycardia, which was inducible and sustained in 15 patients at control, was still inducible after intravenous sotalol in 14 patients, including one in whom it was not inducible at control. However, tachycardia became nonsustained in 10 patients. In seven patients who underwent repeat drug testing while on oral sotalol, results were the same as after intravenous sotalol. Sixteen patients were followed-up for 36 months (median value). Fifteen of them were clinically free of symptoms or experienced marked improvement, despite recurrences of tachycardia in two. In a third patient sotalol had to be withdrawn because of recurrent supraventricular tachycardia. Orthostatic hypotension occurred in five patients and required withdrawal of sotalol in one. To predict the long-term clinical outcome of patients, exercise testing and Holter monitoring were of little or no value. Programmed electrical stimulation predicted clinical outcome in 63% after intravenous and in 86% after oral sotalol. This study shows that long-term treatment with sotalol is highly effective in patients with the Wolff-Parkinson-White syndrome and regular supraventricular tachycardia.
The preventive effect of verapamil on ethanol-induced cardiac depression: phosphorus-31 nuclear magnetic resonance and high-pressure liquid chromatographic studies of hamsters.
Authors: Wu S , White R , Wikman-Coffelt J , Sievers R , Wendland M , Garrett J , Higgins C B , James T , Parmley W W
Published: June 2011

Alcoholic depression of left ventricular function was produced in normal hamsters by the administration of increasing concentrations of alcohol in drinking water (up to 50%) for 6 months. The result was assessed by phosphorus-31 nuclear magnetic resonance of isolated perfused hearts and high-pressure liquid chromatography of freeze-clamped tissues. Hemodynamic data and myocardial oxygen consumption were also monitored. Alcoholic hamsters had significantly higher inorganic phosphate and lower ATP levels, while maintaining normal intracellular pH, phosphocreatine, and creatine. Although coronary flow and oxygen consumption were maintained at normal levels, hamsters ingesting 50% ethanol had significantly lower left ventricular developed pressure and dP/dt. Treatment with verapamil during long-term ethanol consumption prevented the development of these metabolic and functional abnormalities. It is hypothesized that alcohol produces membrane abnormalities leading to adverse ion flux, and that these are largely prevented by concurrent administration of verapamil.
Influence of aortic valve disease on systolic stiffness of the human left ventricular myocardium.
Authors: Wisenbaugh T , Elion J L , Nissen S E
Published: June 2011

The new concept of systolic myocardial stiffness was applied to the study of ejection mechanics in aortic valve disease. Frame-by-frame analysis of stress (sigma) and volume (V) was performed for two differently loaded beats in 26 patients who underwent simultaneous cineangiography and micromanometry: nine normal subjects, eight with isolated aortic regurgitation (AR), and nine with aortic stenosis (AS). Maximum myocardial stiffness (maxEav) was defined as the slope of the end-systolic (es) stress-strain relationship. End-systole was defined as the frame where stiffness was maximal, and strain was defined as epsilon = loge (Dm/Dom), where Dm is left ventricular midwall diameter and Dom is the theoretical Dm at zero stress. Expressed in terms of cavity volume, epsilon = gamma X loge (V/Vo), where gamma is the geometric factor relating Dm to V during systole. Vo was obtained by extrapolating to sigma es = 0 the function, sigma es = maxEav X gamma X loge (Ves/Vo), which was fit to the end-systolic data. Vo always had a value greater than zero. MaxEav was preserved in the AR group (1575 +/- 565) and increased in the AS group (1877 +/- 544; p = .02) compared with normal (1320 +/- 268), suggesting maintenance of contractile force per unit of myocardium in these two lesions. However, theoretical "unloaded" shortening fraction (SFo) was depressed in the AS group (0.30 +/- 0.06; p = .01) compared with normal (0.37 +/- 0.04), preserved in the AR group (0.34 +/- 0.07; p = .24), and inversely related to maxEav (r = -.66, p = .01), suggesting a disparity between shortening potential and force potential.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiovascular mortality and noncontraceptive use of estrogen in women: results from the Lipid Research Clinics Program Follow-up Study.
Authors: Bush T L , Barrett-Connor E , Cowan L D , Criqui M H , Wallace R B , Suchindran C M , Tyroler H A , Rifkind B M
Published: June 2011

A cohort of 2270 white women, aged 40-69 years at baseline, were followed for an average of 8.5 years in the Lipid Research Clinics Program Follow-up Study. There were 44 deaths due to cardiovascular disease among the 1677 nonusers of estrogens and six cardiovascular disease deaths among the 593 estrogen users. The age-adjusted relative risk (RR) of cardiovascular disease deaths in users compared with nonusers was 0.34 (95% confidence limits 0.12 to 0.81). After multivariable adjustment for potential confounding factors (age, blood pressure, and smoking), the estimated RR for estrogen use was 0.37 (95% confidence limits 0.16 to 0.88). Analyses were done to explore whether these results could be due to selection bias for estrogen use. However, the prevalence of cardiovascular disease at baseline was slightly higher in estrogen users (12%) than in nonusers (10%); furthermore, the exclusion of all women with prevalent cardiovascular disease at baseline did not alter the apparent protective effect of estrogen use on cardiovascular disease mortality (RR = 0.42, 95% confidence limits 0.13 to 1.10). Additional analyses examining the complex association between estrogen use, lipoprotein levels, and cardiovascular disease mortality suggest that the protective effect of estrogen is substantially mediated through increased high-density lipoprotein levels.
Increased plasma concentration of cross-linked fibrin polymers in acute myocardial infarction.
Authors: Francis C W , Connaghan D G , Scott W L , Marder V J
Published: June 2011

Thrombin cleaves fibrinopeptides from fibrinogen, converting it to fibrin monomer, and activates factor XIII, which catalyzes the formation of intermolecular epsilon-(gamma-glutamyl)-lysine bonds to stabilize the fibrin polymer. The formation of factor XIIIa-catalyzed fibrin polymers during clotting of plasma and purified fibrinogen in vivo was followed by a sodium dodecyl sulfate agarose gel technique, and an increase in both amount and size of gamma-chain cross-linked polymers was demonstrated before visible clot formation. Plasma from patients presenting with acute myocardial infarction showed increases in the plasma concentration of fibrin polymer and in the proportion of total fibrinogen present as polymer, as determined by a quantitative adaptation of the electrophoretic technique. The plasma concentration in patients with subendocardial or transmural myocardial infarction showed significant (p less than .005) increases to 4.0 +/- 1.0% and 3.6 +/- .8%, respectively, as compared with the concentration in normal plasma (0.8 +/- 0.1%). There was no difference in plasma concentration in samples from patients with transmural compared with those with subendocardial myocardial infarction. This study provides the first demonstration of factor XIIIa cross-linked fibrin polymers in thrombotic disease and indicates the presence of increased activity of both thrombin and factor XIIIa in patients with acute myocardial infarction.
Diastolic function in patients with severe heart failure: comparison of the effects of enoximone and nitroprusside.
Authors: Herrmann H C , Ruddy T D , Dec G W , Strauss H W , Boucher C A , Fifer M A
Published: June 2011

To assess whether the phosphodiesterase inhibitor enoximone has a specific, direct effect on left ventricular diastolic function distinct from its inotropic and vasodilator actions, we compared the effects of enoximone and the pure vasodilator nitroprusside in 11 patients with severe heart failure. Mean (+/- SEM) left ventricular ejection fraction was 0.20 +/- 0.03. Simultaneous left ventricular pressure and radionuclide angiographic volume were obtained at baseline, during infusion of nitroprusside, and after intravenous administration of enoximone. Left ventricular end-diastolic pressure (LVEDP) and volume (LVEDV) decreased with both agents (p less than .01 vs control); LVEDP was lower for nitroprusside than for enoximone (p less than .01) despite a similar LVEDV. Nitroprusside decreased the time constant of exponential left ventricular pressure decay, TL (measured by the logarithmic method), from 84 +/- 10 to 65 +/- 8 msec (p less than .01) but had no significant effect on TD (measured by the derivative method), maximum negative dP/dt, or the peak rate of early diastolic filling. Enoximone shortened TL from 86 +/- 12 to 61 +/- 9 msec (p less than .01) and increased maximum negative dP/dt from 897 +/- 101 to 1135 +/- 134 mm Hg/sec (p less than .01) but did not affect TD or the peak filling rate. The left ventricular diastolic pressure-volume relation was shifted downward in only three of 11 patients on nitroprusside and three of 11 patients on enoximone, and these shifts were attenuated by adjusting for simultaneous changes in right atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
The importance of defining left ventricular area at risk in vivo during acute myocardial infarction: an experimental evaluation with myocardial contrast two-dimensional echocardiography.
Authors: Kaul S , Glasheen W , Ruddy T D , Pandian N G , Weyman A E , Okada R D
Published: June 2011

Because the left ventricular "area at risk" is the most important determinant of ultimate infarct size, it would be useful to know the size of the area at risk during acute myocardial infarction to make therapeutic decisions. We therefore performed a series of experiments in four groups of dogs. In group I dogs (n = 15) we attempted to determine whether current methods of assessing left ventricular function during acute myocardial infarction reflect the true size of the area at risk. At each of two to five sequential stages, a more proximal coronary occlusion was performed to produce a larger area at risk until cardiovascular collapse occurred. At each stage, the area at risk (measured by myocardial contrast echocardiography), hemodynamic variables, and left ventricular ejection fraction (LVEF) were measured. Hemodynamic variables became abnormal when the area at risk was large (25% to 40% of the left ventricle), whereas LVEF became abnormal when the area at risk was of moderate size (18%). When cardiac output and LVEF were normalized to baseline values, a close inverse relationship was noted between these variables and area at risk. In contrast, there was a poor relationship between normalized mean arterial pressure and area at risk (r = .42). In group II dogs (n = 9) the area at risk was measured serially over 6 hr after coronary occlusion. The size of the area at risk remained unchanged regardless of the transmural extent of the ultimate infarct. The circumferential endocardial extent of the area at risk closely predicted the circumferential endocardial extent of the infarct at 6 hr in eight of nine dogs that developed an infarct. Group III dogs (n = 7) underwent the same protocol as group II dogs, but the duration of occlusion was 3 hr. The circumferential endocardial extent of the area at risk closely predicted the circumferential endocardial extent of the infarct. Group IV dogs (n = 5) underwent subtotal coronary occlusion. Although regional wall motion abnormalities were noted in this group, no area at risk could be defined. We conclude that although a close inverse relationship is noted between normalized cardiac output and area at risk, the absolute values for cardiac output and other hemodynamic variables become abnormal only when the area at risk is large (25% to 40%); measurement of LVEF may provide a better assessment of the size of the area at risk than hemodynamic variables.(ABSTRACT TRUNCATED AT 400 WORDS)
The end-systolic pressure-volume relationship in conscious dogs.
Authors: Spratt J A , Tyson G S , Glower D D , Davis J W , Muhlbaier L H , Olsen C O , Rankin J S
Published: June 2011

The end-systolic pressure-volume relationship (ESPVR) has been shown to be an afterload-insensitive descriptor of ventricular inotropic state in the isolated heart. The purpose of this study was to examine the effects of changes in afterload, heart rate, intravascular volume, autonomic tone, and inotropic state on the ESPVR in conscious dogs. In 30 dogs, left ventricular and pleural pressures were measured with micromanometers, and left ventricular volume was assessed with global ultrasonic crystals. The ESPVR was obtained during vena caval occlusions in each dog during pharmacologic afterload interventions at control and after autonomic blockade. Analysis of variance techniques were used to compare the slopes (Emax) and intercepts (Vd) of ESPVR regression lines in a given study. All estimates of the ESPVR in conscious dogs involved large extrapolations to obtain estimates of Vd. Repeat determinations of Emax at control in the unblocked state were significantly different in six of eight dogs (p less than .05). After autonomic blockade, these differences were significant in only one of eight dogs. Changes in heart rate and volume loading had minimal effects on the ESPVR. In the absence of autonomic blockade, increases in inotropic state with either calcium or dobutamine tended to cause parallel shifts in the ESPVR. After autonomic blockade, Emax increased with augmentation of inotropic state, while Vd was unchanged. ESPVRs obtained at different afterloads showed statistically significant differences in Emax and in Vd in 12 of 14 dogs. However, no statistically significant relationship of Emax to afterload was observed. Thus, the ESPVR is probably valid in conscious dogs, but measurement with an intact cardiovascular system is hampered by statistically significant variability in Emax and Vd with changes in afterload. Baseline variability is magnified by the autonomic nervous system, probably mediated through sympathetic reflexes.
Frequency analysis of the surface electrocardiogram for recognition of acute rejection after orthotopic cardiac transplantation in man.
Authors: Haberl R , Weber M , Reichenspurner H , Kemkes B M , Osterholzer G , Anthuber M , Steinbeck G
Published: June 2011

Recognition of acute rejection after heart transplantation has been based mainly on invasive methods until now. In this study we analyzed two well-defined surface electrocardiographic recordings by fast Fourier transform (FFT) (Blackman Harris window, 512 points) after low-noise, high-gain amplification (filter setting 0.5 to 300 Hz) each day for 4 weeks after cardiac transplantation in 27 patients. Twenty acute rejection crises requiring treatment were diagnosed by cytoimmunologic monitoring and endomyocardial biopsy. Single-beat analysis of the QRS complex by FFT revealed a progressive change of the spectral morphology (increase of the frequency content between 70 and 110 Hz) on the days of rejection in 19 of 20 patients. At that time there were no visible changes on the electrocardiogram in the time domain in most patients. At the same time, the frequency content of the ST segment decreased between 10 and 30 Hz in 16 of 20 patients. After successful treatment, the frequency spectra of the QRS complex and ST segment returned to control within 1 to 2 weeks in most patients. One false-positive result was seen in a patient with mediastinitis and large pericardial effusion. A drop in QRS amplitude (greater than 20%) occurred in 10 of 20 rejection crises and in 10 patients without rejection. Nine patients after cardiac transplantation without rejection and seven control patients after cardiac surgery (not transplantation) showed stable frequency plots from one day to the other after the first postoperative day, but with considerable changes in QRS amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)
High-dose calcium channel-blocking therapy for primary pulmonary hypertension: evidence for long-term reduction in pulmonary arterial pressure and regression of right ventricular hypertrophy.
Authors: Rich S , Brundage B H
Published: June 2011

In an attempt to produce substantial reductions in pulmonary arterial pressure and pulmonary vascular resistance in patients with primary pulmonary hypertension, a new treatment strategy using high doses of calcium channel-blocking drugs was developed. Thirteen patients were given an initial test dose of 60 mg diltiazem or 20 mg nifedipine followed by consecutive hourly doses until a 50% fall in pulmonary vascular resistance and 33% fall in pulmonary arterial pressure was achieved or untoward side effects developed. The initial drug challenges failed to produce significant reductions in mean pulmonary arterial pressure or pulmonary vascular resistance. In eight of 13 patients, continued hourly doses produced a reduction in mean pulmonary arterial pressure of 48% (61 to 35 mm Hg, p less than .01) and a reduction in pulmonary vascular resistance of 60% (15 to 6 units, p less than .01). These patients were discharged on high-dose (up to 720 mg/day diltiazem or 240 mg/day nifedipine) calcium channel-blocking drugs as long-term therapy. Five patients have returned for restudy after 1 year. In four of five the reductions in pulmonary arterial pressure and pulmonary vascular resistance were sustained and were associated with regression of right ventricular hypertrophy as assessed by electrocardiography and echocardiography. One patient who reduced her dose to a conventional level had a return of her pulmonary arterial pressure and pulmonary vascular resistance toward previous levels. We conclude that substantial reductions in pulmonary arterial pressure and pulmonary vascular resistance that are associated with regression of right ventricular hypertrophy are possible in some patients with primary pulmonary hypertension by use of calcium channel-blocking drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
Power output of skeletal muscle ventricles in circulation: short-term studies.
Authors: Mannion J D , Acker M A , Hammond R L , Faltemeyer W , Duckett S , Stephenson L W
Published: June 2011

Skeletal muscle ventricles (SMVs) were constructed from preconditioned latissimus dorsi muscles in eight dogs and then connected to each animal's systemic arterial circulation in short-term experiments. The lengths of time that SMVs could produce hemodynamic work as left ventricular assist devices were recorded. After 4 hr of continuous pumping at approximately 55 beats/min, six of eight SMVs were able to generate systolic pressures of 128 +/- 23 mm Hg and flows of 340 +/- 31 ml/min, representing 20 +/- 4% of the animals' cardiac output. After 8 hr of continuous pumping, five of the eight SMVs generated pressures of 110 +/- 15 mm Hg and flows of 308 +/- 88 ml/min, or 15 +/- 7% of the animals' cardiac output. The stroke work produced by the SMVs was intermediate between that of the animals' left and right ventricles. Although the SMVs were stimulated to contract at only about one-third the heart rate, the power output of the SMVs approximated that of the right ventricles because of the greater stroke work of the SMVs. Two SMVs functioned as LVADs for 14 hr. Deterioration in SMV function eventually occurred. In each case, however, complications such as anemia, hypoxia, and hypotension, which are inherent to prolonged short-term experiments of this type, contributed to the deterioration of SMV function. The results presented here suggest that skeletal muscle has the potential to directly support the circulation; however, the length of time such muscle pumps are capable of functioning has yet to be determined.
Blood velocity distribution in the human ascending aorta.
Authors: Segadal L , Matre K
Published: June 2011

Mapping of blood velocities across the lumen of the ascending aorta was performed in eight patients during open-heart surgery. A Doppler ultrasound probe was constructed to measure velocities in 2 mm steps from the maximum convexity to the maximum concavity of aorta, 6 to 7 cm above the aortic valve. In five patients with angina and normal aortic valves, velocity profiles were very similar and showed the following main features: a skewed peak systolic velocity profile with the highest velocity along the left posterior wall, a bidirectional velocity profile in late systole and early diastole with retrograde velocities along the left posterior wall, and a sustained antegrade flow along the convexity well into diastole. The resultant mean velocity profile had the highest velocity at the convex side and a central minimum velocity. In patients with Medtronic-Hall tilting disc prostheses, where the larger opening was oriented backwards and to the right, mean flow velocity profile was skewed in the opposite direction of normal. Moreover, instant systolic velocity profiles were much more irregular and dependent on the exact orientation of the prosthesis. In one patient with aortic valvular disease, very irregular and different velocity profiles were found. Based on a symmetry assumption, overall mean velocity for the total cross section was computed, and the magnitude of error in estimation of total flow from measurement of velocities at different depths was calculated. To measure total flow in the aorta, i.e., cardiac output, by single-gated Doppler technique, the most representative sampling site was about one-third of the diameter from the convex wall.
HLA-A, B, DR, and DQ antigens in black patients with severe chronic rheumatic heart disease.
Authors: Maharaj B , Hammond M G , Appadoo B , Leary W P , Pudifin D J
Published: June 2011

To determine whether genetic factors could be involved in the pathogenesis of rheumatic heart disease, we performed HLA-A and HLA-B typing in 120 black patients with severe chronic rheumatic heart disease requiring cardiac surgery, and HLA-DR and HLA-DQ typing in 103 and 97 of these patients, respectively. The HLA typing was done by a standard microlymphocytotoxicity method. Patients were 12 to 60 years old (mean 27.6 +/- 14.5). No differences in HLA-A, HLA-B, and HLA-DQ frequencies between patients and controls were noted. HLA-DR 1 antigen was present in 12.6% of patients compared with 2.7% of normal control subjects (corrected p less than .045; relative risk = 5.2) and the HLA-DRw6 antigen was present in 31.1% of patients compared with 15% of control subjects (corrected p less than .045; relative risk = 2.6). These findings suggest that genetically determined immune-response factors may play a role in the pathogenesis of severe chronic rheumatic heart disease.
Prevention of ventricular tachycardia induction during right ventricular programmed stimulation by high current strength pacing at the site of origin.
Authors: Marchlinski F E , Buxton A E , Miller J M , Josephson M E
Published: June 2011

To determine whether high current strength pacing at the site of origin of ventricular tachycardia (VT) could prevent induction of VT, we studied 11 VTs in 10 patients with chronic coronary artery disease. The left ventricular site of origin of all VT was determined by endocardial catheter mapping. Reproducible VT induction from the right ventricular apex or outflow tract was demonstrated with a pacing current strength equal to twice diastolic threshold (less than or equal to 2.0 mA) with single (two VTs), double (eight VTs), or triple (one VT) extrastimuli following 8 beats of a drive cycle length of 400 to 600 msec. After determination of the baseline VT induction zone (range 10 to 80 msec), repeat induction was attempted while simultaneous pacing was performed during the 8 beat drive train from the left ventricular site of origin with the use of a high current strength (10 mA [two VTs] or 20 mA [nine VTs]) and from the baseline right ventricular site with a current strength equal to twice diastolic threshold. Extrastimuli were introduced only from the right ventricular site over the same range of coupling intervals that resulted in VT initiation during the baseline state. In five of the 11 trials, no VT could be initiated; in one trial, the VT induction zone was decreased from 80 to 10 msec; in three trials, only VT of a different morphology and a distinct (greater than 4 cm distant) site of origin was initiated; and in two trials, VT of the same morphology was initiated. In four of the five trials in which all VT was prevented by simultaneous pacing with a high current strength at the site of origin, simultaneous pacing at a lower current strength (twice diastolic threshold) at the site of origin (three VTs) or with equally increased current strength (10 to 20 mA) at nonsites of origin (two VTs) did not prevent initiation. We conclude that: high current strength pacing at the site of origin during the drive train can inhibit VT induction with extrastimuli and, successful prevention of VT may depend on the pacing site being the site of origin and the current strength used during pacing.
Dietary therapy for different forms of hyperlipoproteinemia.
Authors: Grundy S M
Published: June 2011

Diet is the first line of therapy for hypercholesterolemia. The major dietary factors raising the plasma cholesterol are saturated fatty acids, cholesterol, and excess total calories. For almost all forms of hyperlipidemia, the first principle of dietary therapy is to reduce saturated fatty acids, decrease cholesterol, and curtail excess calories. In patients with severe hypercholesterolemia, marked restrictions of diet may be necessary. For these patients, drugs may be required to control cholesterol levels. However, the majority of patients with elevated plasma cholesterol can achieve a satisfactory reduction of cholesterol levels by diet, and drugs will not be necessary. Dietary therapy alone is adequate for most patients with familial forms of hypertriglyceridemia, but for a few patients drugs are required.
Delineation of myocardial oxygen utilization with carbon-11-labeled acetate.
Authors: Brown M , Marshall D R , Sobel B E , Bergmann S R
Published: June 2011

Although positron-emission tomography (PET) with labeled fatty acid delineates infarct size and permits qualitative assessment of fatty acid utilization, quantification of oxidative metabolism is limited by complex alterations in the pattern of utilization of fatty acid during ischemia and reperfusion. Because metabolism of acetate by myocardium is less complex than that of glucose or palmitate, we characterized kinetics of utilization of radiolabeled acetate in 37 isolated rabbit hearts perfused with modified Krebs-Henseleit buffer and performed a pilot tomographic study in man. Results of initial experiments with carbon-14-labeled acetate (14C-acetate) indicated that the steady-state extraction fraction of acetate averaged 61.5 +/- 4.0% in control hearts (n = 4), 93.6 +/- 0.9% in hearts rendered ischemic (n = 4), and 54.8 +/- 4.0% in hearts reperfused after 60 min of ischemia (n = 3). Oxidation of 14C-acetate, assessed from the rate of efflux of 14CO2 in the venous effluent, correlated closely with the rate of oxygen consumption under diverse metabolic conditions (r = .97, p less than .001). In addition, no significant differences were observed between rates of efflux of total 14C in all chemical species (reflecting total clearance of tracer from myocardium) and efflux of 14CO2. Clearance of 11C-acetate, measured externally with gamma probes in normal and ischemic myocardium, correlated closely with clearance of 14C-acetate measured directly in the effluent (r = .99, p less than .001) and with overall myocardial oxygen consumption (r = .95, p less than .001). Accumulation and clearance of 11C-acetate from human myocardium with PET demonstrated kinetics comparable to those seen with radiolabeled acetate in vitro. Thus externally detectable clearance of 11C-acetate provides a quantitative index of myocardial oxidative metabolism despite variation in the patterns of intermediary metabolism that confounds interpretation of results with conventionally used tracers such as glucose and fatty acid.
Quantitative determination of aortic regurgitant volumes in dogs by ultrafast computed tomography.
Authors: Reiter S J , Rumberger J A , Stanford W , Marcus M L
Published: June 2011

Current imaging modalities can provide only a qualitative or semiquantitative measure of the severity of aortic regurgitation. Ultrafast computed tomography (CT) has the capability of rapid imaging (17 frames/sec) coupled with high spatial resolution (1.5 mm2). Eight millimeter thick images can be acquired to interrogate simultaneously the right and left ventricles. End-diastolic and end-systolic tomograms can be reconstructed serially from apex to base by Simpson's rule to provide end-diastolic and end-systolic volumes from which the right and left ventricular stroke volumes can be derived. To determine whether the difference between left and right ventricular stroke volume measured with ultrafast CT could be used to estimate the volume of experimentally induced aortic regurgitation, we studied six dogs in which proximal aortic electromagnetic flow probes had been implanted. Varying degrees of aortic regurgitation were induced by manipulation of a basket catheter through the aortic valve. During suspended respiration in the control state in the absence of aortic regurgitation, right and left ventricular stroke volumes measured with ultrafast CT were nearly identical (mean difference 1.0 +/- 1.2 ml [mean +/- SE]). In the presence of varying degrees of aortic regurgitation, regurgitant volume derived by ultrafast CT as the difference between right and left ventricular stroke volumes correlated closely to the regurgitant volume measured by the electromagnetic flow probe (r = .99, slope = .92, y intercept = 0.98 ml, SEE = 1.02 ml, n = 16). Regurgitant fraction also correlated closely to the regurgitant fraction measured by the electromagnetic flow probe (r = .94, slope = .98, y intercept = 0.66%, SEE = 4.73%, n = 16).(ABSTRACT TRUNCATED AT 250 WORDS)
The transstenotic pressure gradient trend as a predictor of acute complications after percutaneous transluminal coronary angioplasty.
Authors: Redd D C , Roubin G S , Leimgruber P P , Abi-Mansour P , Douglas J S , King S B
Published: June 2011

The transstenotic pressure gradient recorded during coronary angioplasty (PTCA) reflects the dynamic relationship that exists between coronary blood flow and the effective cross-sectional area of the arterial lumen. An apparent relationship between the dynamic behavior of the pressure gradient and subsequent acute vessel closure was observed in our catheterization laboratory. We therefore examined the usefulness of the pressure gradient trend in predicting acute complications after 463 attempted PTCA procedures. Two pressure gradient trend patterns were identified: (1) a rising trend pattern identified by an increasing pressure gradient in the interval after deflation of the angioplasty, and (2) a stable trend pattern identified by a constant or decreasing pressure gradient. The incidence of acute vessel closure (17% vs 4%, p = .0001), emergency CABG (5.6% versus 1%, p less than .05), and myocardial infarction (13% versus 2%, p less than .0001) after the PTCA procedure was significantly higher among patients with rising trend patterns when compared with patients with stable trend patterns. Multivariate analysis identified independent predictors for an acute closure event as rising trend pattern (p less than .001), post-PTCA gradient (p less than .05), and post-PTCA percent diameter stenosis (p less than .02). Independent predictors for emergency coronary artery bypass grafting and myocardial infarction were post-PTCA gradient (p less than .001) and a rising trend pattern (odds ratio = 2.91, p less than .001), respectively. The dynamic behavior of the gradient trend provides additional useful information about the results of dilatation.(ABSTRACT TRUNCATED AT 250 WORDS)
Two-dimensional ultrasonic tissue characterization: backscatter power, endocardial wall motion, and their phase relationship for normal, ischemic, and infarcted myocardium.
Authors: Fitzgerald P J , McDaniel M D , Rolett E L , Strohbehn J W , James D H
Published: June 2011

To understand the possible differences in reflected ultrasonic energy from normal, ischemic, and infarcted myocardium, we studied 20 open-chest dogs with a commercially available two-dimensional ultrasonic scanner. Echocardiographic radiofrequency images of anterior myocardium were obtained serially during complete coronary occlusion for 2 hr (n = 15) or 5 hr (n = 10), or after temporary coronary clamping for 15 min with release for 1 hr (n = 5). We investigated two variables: the cyclic backscatter power and the phase difference among endocardial wall motion (EWM), cyclic backscatter power (BSP), and left ventricular pressure (LVP). The cyclic BSP decreased from a control (nonischemic) level of 5.1 +/- 0.8 to 2.3 +/- 0.7 dB during ischemia (up to 30 min after coronary ligation). The phase difference between the EWM and BSP progressed from a control (nonischemic) value of 38 +/- 20 to 115 +/- 23 degrees during ischemia. For the infarction period (2 to 5 hr after coronary ligation), the cyclic BSP progressively returned toward baseline control levels to 4.0 +/- 1.2 dB, but the phase had increased further to 170 +/- 28 degrees. The reperfusion study showed a similar decrease in cyclic BSP and an increase in phase after arterial clamping and both returned to near-normal nonischemic values upon arterial release. Simultaneous LVP recordings were performed to assess the phase contribution of endocardial dyskinesis to the total phase difference measurement. At 5 hr the dyskinesis had contributed 46% to the total phase difference, while the backscatter power contributed 54%. However, the EWM contribution occurred immediately while BSP contribution changed progressively during the 5 hr study period.(ABSTRACT TRUNCATED AT 250 WORDS)
Determinants of induced sustained arrhythmias in survivors of out-of-hospital ventricular fibrillation.
Authors: Swerdlow C D , Bardy G H , McAnulty J , Kron J , Lee J T , Graham E , Peterson J , Greene H L
Published: June 2011

We prospectively studied 196 consecutive survivors of out-of-hospital ventricular fibrillation (VF) not associated with acute myocardial infarction and 46 consecutive, control patients without prior ventricular arrhythmias. Programmed stimulation included two extrastimuli (S3 protocol) in all patients and three extrastimuli (S4 protocol) in the last 140 study patients and in all control patients. Sustained ventricular tachycardia (VT) or VF was not induced in any control patient. In study patients, logistic regression identified two independent predictors of induced, sustained VT for both S3 and S4 protocols: prior spontaneous, sustained VT (37 patients; p less than or equal to .001) and prior myocardial infarction (113 patients; p = .005). With the S3 protocol, sustained VT was induced in 54% of patients with both prior myocardial infarction and prior sustained VT vs 4% without either; with the S4 protocol, sustained VT was induced in 91% vs 13%, respectively. Eighty-three percent of induced VT episodes had a cycle length less than 300 msec, and all required termination by cardioversion or pacing. VF was induced only in survivors of out-of-hospital VF without prior, spontaneous, sustained VT (S3 protocol, 9%; S4 protocol, 24%) but not in study patients with prior sustained VT (S3, p = .10; S4, p = .05) or control patients (S3, p = .06; S4, p = .01). The mean coupling intervals of extrastimuli that induced VF were not significantly different from the intervals that induced sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)
Intermittent claudication, exercise, and blood rheology.
Authors: Ernst E E , Matrai A
Published: June 2011

Forty-two stable patients with claudication were assigned to two groups. Group I (n = 22) was submitted to regular, standardized treadmill exercise for 2 months. During this time the maximal and pain-free walking distances increased significantly (more than 100%). Group II (n = 20) patients did not exercise over the same period of time, and their walking distances remained essentially unchanged. No drugs or other forms of treatment were given in either group. The rheology of blood, as quantified by blood and plasma viscosity, hematocrit, blood filterability, and red cell aggregation, was initially abnormal in patients as compared with matched controls. Blood and plasma viscosity, blood cell filterability, and red cell aggregation normalized significantly in group I, but remained pathologic in group II. The hemorrheologic values of patients after 2 months of exercise did no longer differ significantly from those of healthy controls. The "fluidification" of blood induced by regular exercise was qualitatively and quantitatively similar to that obtainable by hemorrheologically active medications. The results confirm that physical training is clinically effective in patients suffering from claudication. They furthermore suggest that training may be looked on as a form of "hemorrheologic therapy" suitable for increasing the fluidity of blood in patients with ischemic diseases. Part of the benefits of regular exercise in stage II occlusive peripheral arterial disease may result from changes in hemorrheology; further studies are needed to define the mechanism.
Regional effects of verapamil on recovery of excitability and conduction time in experimental ischemia.
Authors: Kimura S , Bassett A L , Kohya T , Kozlovskis P L , Myerburg R J
Published: June 2011

This study was designed to test the hypothesis that verapamil has an effect on ischemia-initiated arrhythmias related to its regional influences on recovery of excitability and conduction time. Using a coronary perfused preparation of cat left ventricle that allows simultaneous electrophysiologic monitoring of both endocardium and epicardium, we studied the effect of verapamil on ischemia-induced changes in transmembrane action potentials, conduction properties, and refractory periods of endocardial and epicardial muscle cells. Oxygenated Tyrode's solution was perfused through the left anterior descending coronary artery, while the preparation was superfused with Tyrode's solution gassed with 95% N2 and 5% CO2. "Ischemia" was produced by stopping coronary perfusion. During 30 min of ischemia, resting potential, action potential amplitude (APA), and action potential duration (APD) were reduced, and conduction time was prolonged in both endocardial and epicardial cells, but the changes were greater in the epicardial cells. Endocardial refractory periods shortened in parallel with APD shortening throughout 30 min of ischemia, whereas epicardial refractory periods shortened for the first 10 min and then increased due to development of longer postrepolarization refractoriness. As a result, there were significant differences in refractory periods between endocardial and epicardial cells at 10 and 30 min of ischemia, and rapid ventricular activity could be induced at these times. Exposure to verapamil (1 mg/liter) before cessation of coronary perfusion significantly limited the reduction of APA and the prolongation of conduction time during the first 10 min of ischemia in epicardial cells, but did not influence endocardial cells. During the remaining 20 min of ischemia, verapamil enhanced the reduction of APD of both epicardial and endocardial cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of pacing-induced ischemia on early left ventricular filling and regional myocardial dynamics and their modification by nifedipine.
Authors: Nakamura Y , Sasayama S , Nonogi H , Miyazaki S , Fujita M , Kihara Y , Konishi T , Kawai C
Published: June 2011

The effect of pacing-induced ischemia on early left ventricular filling and regional myocardial lengthening was studied in 11 patients with coronary artery disease (CAD) and six control patients with normal coronary arteriograms. All of the 11 patients with CAD developed typical anginal pain during pacing tachycardia, and in the postpacing beat, the left ventricular end-diastolic pressure (LVEDP) rose from 13 +/- 4 to 26 +/- 4 mm Hg (mean +/- SD, p less than .01), the relaxation time constant increased from 43 +/- 9 to 59 +/- 7 msec (p less than .01), and the ejection fraction diminished from 62.1 +/- 6.7 to 51.6 +/- 10.6% (p less than .01). However, the peak rate of early left ventricular filling (LVPF) obtained from frame-by-frame analysis of left ventriculograms and the LVPF normalized for the stroke volume and for the end-diastolic volume did not change significantly. In the ischemic segment, the peak rate of lengthening (PL) decreased by 45% with ischemia, and the PL normalized for the end-diastolic segment length decreased by 42%. However, the PL normalized for the extent of systolic shortening did not change. In the control segment there was a tendency for these three variables to increase, but the changes were not statistically significant. The time difference from the PL to the LVPF increased significantly in the ischemic segment (31 +/- 28 vs 75 +/- 48 msec, p less than .05). Although the LVEDP rose slightly but significantly from 9 +/- 3 to 12 +/- 5 mm Hg (p less than .05) in the control patients in the postpacing beat, the other global hemodynamic variables and the variables of regional myocardial dynamics did not change. The administration of nifedipine in six patients with CAD resulted in the disappearance or diminution of anginal pain even with the same duration and rate of pacing and was associated with restoration of global systolic function and regional myocardial shortening and lengthening in the ischemic segment. In the control segment, the three variables of segmental lengthening increased with administration of nifedipine. Thus, the segmental myocardial lengthening rate decreased with ischemia due to a decrease in segmental shortening and impairment of myocardial distensibility. The LVPF did not decrease with ischemia despite impairment in isovolumetric relaxation, accentuation of asynchrony in left ventricular filling, and a decrease in the PL in the ischemic segment because of an increase in the PL in the nonischemic segment secondary to an increase in left ventricular filling pressure.(ABSTRACT TRUNCATED AT 400 WORDS)
Combined percutaneous aortic valvuloplasty and transluminal coronary angioplasty in adult patients with calcific aortic stenosis and coronary artery disease.
Authors: McKay R G , Safian R D , Berman A D , Diver D J , Weinstein J S , Wyman R M , Cunningham M J , McKay L L , Baim D S , Grossman W
Published: June 2011

Of 120 consecutive balloon aortic valvuloplasty procedures for critical aortic stenosis, valvuloplasty was performed in combination with coronary angioplasty in nine patients (average age 76 years). All nine patients were symptomatic with angina and congestive heart failure before combined procedures. Aortic valvuloplasty was performed with 20 to 23 mm balloon catheter advanced retrogradely from the femoral artery and resulted in an improvement in peak aortic valve gradient (60 +/- 19 to 33 +/- 13 mm Hg; p less than or equal to .01) and calculated aortic valve area (0.7 +/- 0.1 to 1.1 +/- 0.3 cm2; p less than or equal to .01). Single-vessel coronary angioplasty was performed via the femoral approach, with 2.0 to 3.5 mm balloon catheters, and resulted in a mean reduction of a critical coronary stenosis in each patient from 91 +/- 4% to 29 +/- 8%. The site of coronary angioplasty was the left anterior descending artery in three patients, the circumflex artery in three patients, the right coronary artery in two patients, and a bypass graft to the right coronary artery in one patient. Combined procedures were performed with a mean arterial time of 108 min. Complications included groin hematomas (n = 2), transient left bundle branch block (n = 1), and transient atrial fibrillation (n = 1). No patient experienced prolonged chest pain, myocardial infarction, major increase in aortic insufficiency, or embolic phenomena. Eight of the nine patients treated with combined procedures noted significant improvement in symptoms of angina and congestive heart failure and were discharged.(ABSTRACT TRUNCATED AT 250 WORDS)
Neodymium:YAG laser photocoagulation: a successful new map-guided technique for the intraoperative ablation of ventricular tachycardia.
Authors: Svenson R H , Gallagher J J , Selle J G , Zimmern S H , Fedor J M , Robicsek F
Published: June 2011

Neodymium:YAG laser photocoagulation was used in the intraoperative treatment of drug-resistant ventricular tachycardia (VT) in 17 consecutive patients. The cause of VT was previous myocardial infarction in 15, sarcoid in one, and idiopathic in one patient. Electrophysiologic studies were performed preoperatively, before hospital discharge, and 8 to 12 weeks and 1 year after surgery. At surgery, laser photocoagulation was performed on the normothermic heart during VT. Surgical mortality was 11.7%. There was one late nonarrhythmic death 35 days postoperatively. There were 55 VT morphologies. Laser successfully abated 52 of 55. Associated use of cryoablation was required in two of 55. One VT in the patient with sarcoidosis was not successfully ablated but was controlled by procainamide. In the long-term survivors with VT due to myocardial infarction the surgical cure rate was 100%, i.e., no spontaneous or inducible VT. Follow-up ranges from 6 to 18 months (mean 11.8 +/- 4.3). Nd:YAG laser photocoagulation is an effective addition to the operative treatment strategies for VT.
Cryosurgical treatment of atrioventricular node reentrant tachycardia.
Authors: Cox J L , Holman W L , Cain M E
Published: June 2011

Paroxysmal supraventricular tachycardia most commonly arises from reentry within the atrioventricular (AV) node. Although ablation of the His bundle has gained popularity for treating patients with AV node reentrant tachycardia refractory to medical therapy, undesirable sequelae include complete heart block and the necessity for a permanent pacemaker. To obviate this limitation, we have developed a discrete cryosurgical procedure that interrupts the reentrant circuit responsible for AV node reentrant tachycardia without blocking AV conduction. After first characterizing the salutary effects of this approach in experimental animals, we performed this procedure in eight patients with AV node reentrant tachycardia. Preoperative, intraoperative, and postoperative electrophysiologic studies were performed in each patient. Under conditions of normothermic cardiopulmonary bypass and during atrial pacing at a constant rate with continuous monitoring of AV conduction, nine separate 3 mm cryolesions (-60 degrees C for 2 min) were placed at predetermined sites around the triangle of Koch in the lower right atrial septum. Postoperatively, each patient had a single AV node conduction curve. No patient had AV node reentrant tachycardia induced or has experienced AV node reentrant tachycardia clinically during a follow-up of up to 5 years. The cryosurgical procedure had no detrimental effects on the AH or HV interval or on the paced cycle length at which AV node Wenckebach occurred. Based on these results, this curative operation offers promise for patients with AV node reentrant tachycardia that is refractory to medical treatment.