bluuebunny/crossref_metadata_2025 huggingface dataset:
Detailed angiographic analysis of high-speed mechanical rotational atherectomy in human coronary arteries.
Authors: Safian R D , Niazi K A , Strzelecki M , Lichtenberg A , May M A , Juran N , Freed M , Ramos R , Gangadharan V , Grines C L
Published: June 2012

BACKGROUND

Several types of atherectomy devices have been developed recently for treatment of patients with ischemic heart disease.

METHODS AND RESULTS

Mechanical rotational atherectomy (MRA) using a high-speed rotational burr (Rotablator) was performed on 116 lesions in 104 patients. MRA alone was performed in 27 lesions (23%), and conventional balloon angioplasty (PTCA) was performed after MRA in 89 lesions (77%). Diameter stenosis decreased from 70 +/- 13% before MRA to 54 +/- 23% after MRA, and the final diameter stenosis (after MRA alone or with adjunctive PTCA) was 30 +/- 20% (P < .001). Minimal lumen diameter increased from 1.0 +/- 0.5 mm before MRA to 1.4 +/- 0.7 mm after MRA, and the final minimal lumen diameter was 2.3 +/- 0.7 mm (P < .001). MRA resulted in a decrease in diameter stenosis of 20% or more in 44% of lesions, and the final diameter stenosis (after MRA alone or after PTCA) was less than 50% in 75% of lesions. Considering the small diameter of available burrs, the magnitude of lumen enlargement was equal to 91% of the burr diameter, and only 9% of the burr diameter was "lost" due to elastic recoil or spasm. These angiographic results were obtained despite the presence of complex lesion morphology, including the presence of calcification in 17% of lesions and ostial location in 26% of lesions. Significant angiographic complications included abrupt closure (13 lesions, 11.2%), no reflow (8 lesions, 7%), severe coronary vasospasm (16 lesions, 13.8%), and guide wire fracture (3 lesions, 2.7%). There were no coronary artery perforations. Adjunctive therapy, including salvage PTCA, thrombolytic agents, and vasodilators, was successful in treating angiographic complications in 42 of 49 lesions (86%). Clinical complications included Q-wave myocardial infarction (5 patients, 4.8%), non-Q-wave myocardial infarction (3 patients, 2.9%), femoral vascular injury requiring surgery (3 patients, 2.9%) or blood transfusion (8 patients, 7.7%), abrupt closure requiring emergency bypass graft surgery (2 patients, 1.9%), and in-hospital death (1 patient, 1.0%). Angiographic follow-up (mean follow-up interval, 5.0 +/- 2.0 months) was available in 84% of successfully treated patients and revealed a restenosis rate of 51%, defined as a residual diameter stenosis of more than 50%. There was no significant difference in restenosis rates between de novo lesions (50%) and restenosis (54%) lesions.

CONCLUSIONS

These data suggest that for the treatment of most coronary stenoses, PTCA is required after MRA to achieve satisfactory lumen enlargement or to salvage complications. Angiographic complications appear to be more common after MRA, and salvage PTCA often is required to manage these device-induced complications. The combination of MRA and PTCA does not prevent restenosis.
Restenosis rate after multiple percutaneous transluminal coronary angioplasty procedures at the same site. A quantitative angiographic study in consecutive patients undergoing a third angioplasty procedure for a second restenosis.
Authors: Bauters C , Mc Fadden E P , Lablanche J M , Quandalle P , Bertrand M E
Published: June 2012

BACKGROUND

Several studies suggest that repeated percutaneous transluminal coronary angioplasty procedures at the same site are associated with a progressively increasing risk of further restenosis and that short time intervals between successive procedures are predictive of future restenosis.

METHODS AND RESULTS

We assessed by quantitative coronary angiography the angiographic probability of restenosis when repeat percutaneous transluminal coronary angioplasty was performed at a site where restenosis had occurred after two previous angioplasty procedures. Of 99 consecutive patients who underwent a third angioplasty procedure, 96 had successful procedures. Uncomplicated failure (residual stenosis > or = 50%) occurred in 3 patients. No major complications occurred. Follow-up angiography was routinely advised; it was performed in 83 patients (86%) with successful procedures. Restenosis (recurrence of > or = 50% stenosis determined by quantitative coronary angiography) occurred in 32 patients (39%). An interval of < 3 months between the second and third angioplasty was strongly associated (P < .005) with the occurrence of further restenosis after a third procedure.

CONCLUSIONS

The angiographic probability of further restenosis after three successive angioplasty procedures at the same site is similar to that reported after a first angioplasty procedure in studies that used a similar definition of restenosis. Patients who undergo a third angioplasty procedure within 3 months of a previous procedure at the same site have a much higher risk of subsequent restenosis. This easily identified subgroup may benefit from an alternative therapeutic approach.
Effects of age and aerobic capacity on arterial stiffness in healthy adults.
Authors: Vaitkevicius P V , Fleg J L , Engel J H , O'Connor F C , Wright J G , Lakatta L E , Yin F C , Lakatta E G
Published: June 2012

BACKGROUND

It has been well established that arterial stiffness, manifest as an increase in arterial pulse wave velocity or late systolic amplification of the carotid artery pressure pulse, increases with age. However, the populations studied in prior investigations were not rigorously screened to exclude clinical hypertension, occult coronary disease, or diabetes. Furthermore, it is unknown whether exercise capacity or chronic physical endurance training affects the age-associated increase in arterial stiffness.

METHODS AND RESULTS

Carotid arterial pressure pulse augmentation index (AGI), using applanation tonometry, and aortic pulse wave velocity (APWV) were measured in 146 male and female volunteers 21 to 96 years old from the Baltimore Longitudinal Study of Aging, who were rigorously screened to exclude clinical and occult cardiovascular disease. Aerobic capacity was determined in all individuals by measurement of maximal oxygen consumption (VO2max) during treadmill exercise. In this healthy, largely sedentary cohort, the arterial stiffness indexes AGI and APWV increased approximately fivefold and twofold, respectively, across the age span in both men and women, despite only a 14% increase in systolic blood pressure (SBP). These age-associated increases in AGI and APWV were of a similar magnitude to those in prior studies of less rigorously screened populations. Both AGI and APWV varied inversely with VO2max, and this relationship, at least for AGI, was independent of age. In endurance trained male athletes, 54 to 75 years old (VO2max = 44 +/- 3 mL.kg-1.min-1), the arterial stiffness indexes were significantly reduced relative to their sedentary age peers (AGI, 36% lower; APWV, 26% lower) despite similar blood pressures.

CONCLUSIONS

Even in normotensive, rigorously screened volunteers in whom SBP increased an average of only 14% between ages 20 and 90 years, major age-associated increases of arterial stiffness occur. Higher physical conditioning status, indexed by VO2max, was associated with reduced arterial stiffness, both within this predominantly sedentary population and in endurance trained older men relative to their less active age peers. These findings suggest that interventions to improve aerobic capacity may mitigate the stiffening of the arterial tree that accompanies normative aging.
Prognosis of myocardial infarctions involving more than 40% of the left ventricle after acute reperfusion therapy.
Authors: McCallister B D , Christian T F , Gersh B J , Gibbons R J
Published: June 2012

BACKGROUND

Prior studies based on autopsy data suggest that infarction of more than 40% of the left ventricle necessitates cardiogenic shock and death.

METHODS AND RESULTS

Technetium-99m Sestamibi tomography was used prospectively to measure infarct size at discharge in 166 patients with acute myocardial infarction. Patients with previous myocardial infarction or revascularization were excluded from the trial. Sixteen patients were identified with final infarct sizes > 40% of the left ventricle despite acute reperfusion therapy. These 16 patients (13 men) had a mean age of 63 +/- 10 years; 44% had a previous history of angina. Ten patients had emergent coronary angioplasty only (mean time to percutaneous transluminal coronary angioplasty [PTCA], 6.0 +/- 3.0 hours); 6 had thrombolysis (mean time to tissue plasminogen activator, 4.0 +/- 1.5 hours), of which 2 had rescue PTCA (5 and 3 hours from onset of pain). Of 15 patients who had angiograms after therapy, 15 had open infarct-related arteries. The left anterior descending artery was the infarct-related artery in 14 (9 proximal and 5 distal lesions). Half the patients had only single-vessel disease. Infarct size measured 50 +/- 7% of the left ventricle (range, 42% to 68%). Ejection fraction by radionuclide angiogram was 0.33 +/- 0.09 and 0.38 +/- 0.07 at discharge and 6 weeks, respectively. Hospital complications included shock (1 patient), pulmonary edema (2), angina (3), symptomatic nonsustained ventricular tachycardia (1), transient complete heart block (2), and transient bifascicular block (1). At follow-up (13 +/- 9 months), the patient with shock had died, but the remaining 15 patients were asymptomatic (1 had late PTCA for angina).

CONCLUSIONS

In the interventional and thrombolytic era, patients with large residual myocardial infarctions can survive without heart failure.
Residual flow to the infarct zone as a determinant of infarct size after direct angioplasty.
Authors: Clements I P , Christian T F , Higano S T , Gibbons R J , Gersh B J
Published: June 2012

BACKGROUND

In acute myocardial infarction, residual flow to the infarct zone either through antegrade flow in the infarct-related coronary artery or collateral flow from the non-infarct-related arteries is often present before reperfusion therapy. The purpose of this study was to assess the influence of antegrade flow in the infarct-related artery and/or collateral flow to the infarct zone before successful direct angioplasty on infarct size and myocardial salvage in patients with acute evolving myocardial infarction.

METHODS AND RESULTS

Sixty patients with acute evolving myocardial infarction underwent direct successful angioplasty without prior thrombolytic therapy. The myocardium at risk of infarction, the final infarct size, and myocardial salvage were measured by tomographic perfusion imaging with 99mTc sestamibi. Antegrade flow in the infarct-related artery before intervention was graded according to the Thrombolysis in Myocardial Infarction (TIMI) study group classification. Collateral flow to the infarct zone before angioplasty was also graded (0 through 3, 0 being no collateral flow). The presence of even minimal antegrade flow before angioplasty (TIMI grade 1) in the infarct-related artery compared with absent flow was associated with a significant reduction in final infarct size (9 +/- 17% versus 23 +/- 19% of left ventricle, P = .02) and a significant increase in myocardial salvage (23 +/- 16% versus 14 +/- 13% of left ventricle, P = .05) after angioplasty. When antegrade flow in the infarct-related artery was absent before angioplasty, the presence of collateral flow before angioplasty resulted in a significantly smaller final infarct size (P = .01) and more myocardial salvage (P = .05) after angioplasty. Both antegrade infarct-related artery flow and collateral flow to the infarct zone had significant independent ability to predict infarct size after angioplasty. When collateral grade and TIMI grade were added to provide an estimate of residual flow, a model including residual flow, myocardium at risk, and the interaction of residual flow and infarct site explained 83% of the variability in infarct size after angioplasty.

CONCLUSIONS

The presence of antegrade flow in the infarct-related artery and/or collateral flow to the infarct zone before direct angioplasty in acute evolving infarction results in a smaller infarct size after direct successful angioplasty.
Predicting early and intermediate-term outcome of coronary angioplasty in the elderly.
Authors: Thompson R C , Holmes D R , Gersh B J , Bailey K R
Published: June 2012

BACKGROUND

Although the technical success rate of coronary angioplasty in the elderly in high, very old patients have increased risk of procedure-related death and late recurrence of severe angina. We proposed to determine baseline variables that predict early and intermediate-term failure of percutaneous transluminal coronary angioplasty (PTCA) in patients more than 65 so we could effectively stratify risk.

METHODS AND RESULTS

We studied 982 patients at least 65 years old who had urgent or elective PTCA (1980 through 1990). Follow-up (mean, 25 months) was obtained for all patients. Multiple baseline variables were analyzed with univariate and multivariate logistic regression to select independent ones to fit predictive models for in-hospital death or myocardial infarction (overall rate, 6.3%), total in-hospital adverse outcome (overall rate, 18.7%), cumulative survival free of myocardial infarction (overall rate, 15% at 3 years), and cumulative survival free of late nonfatal myocardial infarction, bypass surgery, repeat PTCA, or recurrent severe angina (overall rate, 47% at 3 years). The most heavily weighted parameter in the probability regression equation for each end point was the number of diseased coronary artery segments with at least 70% stenosis. Advanced age was less important. The number of concomitant medical illnesses was predictive of late outcome but not early in-hospital events. Lowest risk quintile versus highest risk quintile event rate was 2.9% versus 14% for acute myocardial infarction or death and 17.2% versus 29% for cumulative in-hospital events. For posthospital events at 3 years' follow-up, lowest risk quintile death or myocardial infarction rate was 4% versus 33% for highest risk quintile. For cumulative late adverse events at 3 years, the event rate was 28% versus 63% for the highest risk quintile.

CONCLUSIONS

These results stratify patients at high and low risk of early and intermediate-term success after PTCA and identify elderly patients in whom PTCA is most appropriate.
Effects of flecainide on ectopic atrial automaticity and conduction.
Authors: Windle J R , Witt R C , Rozanski G J
Published: June 2012

BACKGROUND

Previous studies have shown that class Ic antiarrhythmic agents are effective in suppressing ectopic atrial rhythms and accessory pathway conduction.

METHODS AND RESULTS

To explore the potential mechanisms for their effectiveness, we investigated the concentration-dependent effects of the Ic agent flecainide acetate (0.5 to 10 micrograms/mL) on atrial ectopic automaticity and exit conduction in isolated rabbit tricuspid valves. This experimental model consists of three major cell types as defined anatomically and by intracellular recordings: pacemaker, transitional, and working atrial muscle. Simultaneous recordings from these cell types before and during flecainide superfusion (n = 7) showed that the drug produced a slight, concentration-dependent slowing of pacemaker-transitional conduction but elicited third-degree transitional-working atrial muscle block in six of seven preparations at 10 micrograms/mL. Flecainide caused a significant dose-dependent reduction in the initial phase of diastolic depolarization of pacemaker cells but produced only a small, biphasic change in spontaneous pacemaker cycle length. It also caused a significant prolongation in action potential duration in pacemaker and transitional cells and reduction in upstroke velocity in atrial cells. Of note in four additional preparations, flecainide caused a concentration-dependent upward shift in the strength-duration curve for atrial fibers.

CONCLUSIONS

These data suggest that flecainide has little direct effect on ectopic atrial automaticity but rather causes exit conduction slowing and block between transitional and atrial muscle fibers. The mechanism for the induction of block is likely due to a decrease in atrial excitability creating a greater electrical load on generated impulses.
Differentiation between aberrant ventricular conduction and ventricular ectopy in atrial fibrillation using RR interval scattergram.
Authors: Suyama A C , Sunagawa K , Sugimachi M , Anan T , Egashira K , Takeshita A
Published: June 2012

BACKGROUND

Differentiation between aberrant ventricular conduction and ventricular ectopy during atrial fibrillation (AF) is of etiologic, prognostic, and therapeutic importance. We developed a noninvasive technique to diagnose aberrant ventricular conduction and ventricular ectopy in AF.

METHODS AND RESULTS

We studied the Holter ECGs of 34 patients with paroxysmal AF and 62 patients with chronic AF. In all the patients, frequent wide QRS complexes were observed, and 32 patients were shown by electrophysiological examination to have ventricular ectopies or aberrant ventricular conductions. We obtained the RR interval scattergrams by plotting sequential pairs of RR intervals. Each point has the (n)th RR interval as its x value and the (n + 1)th RR interval as its y value. The irregularity of the RR intervals in AF resulted in widely scattered points delineated by the envelope along the axes. The y value of the envelope along the x axis indicates the shortest coupling interval to the preceding RR interval. Therefore, this curve defines the functional refractory period of atrioventricular conduction. The scattergram of the RR interval pairs immediately preceding the aberrant conduction (coupling points of aberrant conduction) specifically distributed along the envelope. In contrast, the coupling points of ventricular ectopies showed different distributions that had no relation to the envelope. That is, it included three typical patterns, ie, linear distribution below the envelope, linear distribution partially overlapped in the area of normal AF conduction, and chaotic distribution in the AF area. None of the scattergrams of ventricular ectopies showed curvilinear distribution along the envelope as aberrant conduction did. The specific distribution of the aberrant conduction on the RR interval scattergram suggested that aberrant conduction in AF could result from the difference of refractory periods between the AV node and bundle branch block.

CONCLUSIONS

We conclude that the RR interval scattergram makes it possible to differentiate between aberrant ventricular conduction and ventricular ectopy in atrial fibrillation, and thus, it is a useful noninvasive clinical tool.
Short-term synchronized retroperfusion before reperfusion reduces infarct size after prolonged ischemia in dogs.
Authors: Wakida Y , Nordlander R , Kobayashi S , Kar S , Haendchen R , Corday E
Published: June 2012

BACKGROUND

Previous studies have demonstrated that synchronized coronary venous retroperfusion (SRP) can restore blood flow to the ischemic myocardium, resulting in infarct size reduction and improvement of the left ventricular function. Despite the nutritive blood flow achieved by SRP being relatively limited, SRP has been shown to improve washout of by-products from the ischemic myocardium. The aim of this study was to investigate whether short-term SRP immediately prior to reperfusion would attenuate the deteriorative phenomena following reperfusion.

METHODS AND RESULTS

Closed-chest anesthetized dogs underwent 3 hours of left anterior descending coronary artery (LAD) occlusion. The dogs were then randomized into two groups: (1) control group (n = 9), in which the occlusion was immediately followed by 3-hour reperfusion; or (2) SRP group (n = 9), in which SRP was started 3 hours after occlusion and maintained for 30 minutes with sustained occlusion followed by 2.5-hour reperfusion with simultaneous discontinuation of SRP. There were no statistical differences between the groups in global hemodynamics and degree of ischemia measured by radiolabeled microspheres. Myocardial infarct size (triphenyltetrazolium method) expressed as percentage of risk area was significantly smaller in the SRP group (24 +/- 7%, mean +/- SEM) than in the control group (54 +/- 9%). The extent of myocardial hemorrhage expressed as percentage of infarct size was also significantly reduced in the SRP group (3 +/- 2%) compared with the control group (24 +/- 6%). The increase in end-diastolic wall thickness in the ischemic area after reperfusion assessed by two-dimensional echocardiography was significantly less in the SRP group. Blood flow measurements after reperfusion demonstrated the occurrence of no-reflow phenomenon only in the control group. Histological examination revealed extensive myocardial hemorrhages only in the control group, which extended into the nonnecrotic myocardium in four of nine hearts and extensive contraction band necrosis compared with the SRP group.

CONCLUSIONS

Short-term SRP prior to reperfusion can reduce infarct size, myocardial hemorrhage, wall swelling, and no-reflow phenomenon. The mechanism of this beneficial effect is not clear but might be due to gradual reperfusion and washout of by-products from the ischemic myocardium before fully oxygenated arterial blood reperfusion.
Late reperfusion for acute myocardial infarction limits the dilatation of left ventricle without the reduction of infarct size.
Authors: Hirayama A , Adachi T , Asada S , Mishima M , Nanto S , Kusuoka H , Yamamoto K , Matsumura Y , Hori M , Inoue M
Published: June 2012

BACKGROUND

While previous clinical studies have shown a possible beneficial effect of the reperfusion performed at a relatively late phase of acute myocardial infarction ("late reperfusion") in preventing left ventricular enlargement, the mechanism has not been clarified.

METHODS AND RESULTS

Of 89 patients with an initial anterior myocardial infarction, reperfusion was successful in 69. These 69 were divided into three groups according to the time required to achieve reperfusion after the onset of symptoms: early-reperfused (< 3 hours from the onset to reperfusion; n = 22), intermediate-reperfused (3 to 6 hours from the onset to reperfusion; n = 28), and late-reperfused (> 6 hours from the onset to reperfusion; n = 19). The 20 patients whose infarct-related artery were occluded in the acute phase as well as 1 month later was classified as nonreperfused. Infarct size, evaluated as defect volume by 201Tl single-photon emission computed tomography 1 month after the onset, was 1593 +/- 652 units (mean +/- SD) in the late-reperfused group, significantly larger (P < .05) than that of the intermediate-reperfused (1066 +/- 546 U) or the early-reperfused groups (372 +/- 453 U) but not different from that of the nonreperfused group (1736 +/- 562 U). Wall motion abnormality index as well as global ejection fraction evaluated by left ventriculography 1 month after the onset showed that late reperfusion did not preserve the left ventricular wall motion and function. These results indicate that the earlier reperfusion decreased the size of the infarction and preserved left ventricular function, whereas late reperfusion (> 6 hours after onset) did not limit infarct size or preserve left ventricular function. In contrast, the end-diastolic volume index did not differ significantly among the early-reperfused (50 +/- 15 mL/m2), intermediate-reperfused (54 +/- 14 mL/m2), and late-reperfused (53 +/- 19 mL/m2) groups; those were significantly smaller than that of the nonreperfused group (68 +/- 12 mL/m2; P < .05). Left ventriculographic data obtained in both the acute and chronic phase in 39 patients showed that left ventricular volumes increased significantly during the course of myocardial infarction only in the nonreperfused group.

CONCLUSIONS

Late reperfusion appeared to prevent ventricular dilatation acute myocardial infarction independent of the limitation of infarct size.
Effects of adenosine on rate-dependent atrioventricular nodal function. Potential roles in tachycardia termination and physiological regulation.
Authors: Nayebpour M , Billette J , Amellal F , Nattel S
Published: June 2012

BACKGROUND

Adenosine is well known to depress atrioventricular (AV) nodal conduction, but the potential interactions between adenosine and functional AV nodal properties have not been explored. The purpose of the present study was to determine (1) whether exogenous adenosine modifies the rate-dependent properties of the AV node, (2) to what extent such changes underlie the actions of adenosine in an in vitro model of AV reentrant tachycardia (AVRT), and (3) the potential role of endogenous adenosine in rate-induced AV nodal responses.

METHODS AND RESULTS

The functional properties of AV nodal recovery (defining the conduction delay of a single premature activation), facilitation (effect of short cycles on subsequent nodal recovery), and fatigue (slowly developing AV nodal delay at a rapid rate) were studied selectively in isolated, superfused rabbit and guinea pig cardiac preparations. Exogenous adenosine increased AV nodal fatigue and attenuated facilitation, resulting in tachycardia-dependent increases in AH interval and AV nodal effective refractory period (AVERP). In experimental AVRT, adenosine caused greater increases in tachycardia cycle length (T) and AVERP as tachycardia rate increased. AVRT was sustained when AVERP/T was < 1, and adenosine suppressed AVRT by increasing the slope of the AVERP/T versus tachycardia rate relation, causing the critical ratio of 1 to be attained at slower rates. A mathematical model incorporating quantitative descriptors of recovery, facilitation, and fatigue accounted for changes in AH interval, AVERP, tachycardia cycle length, and AVERP/T under control conditions and in the presence of adenosine. In the absence of exogenous adenosine, 8-phenyltheophylline (10 mumol/L), an adenosine receptor antagonist, did not alter recovery or facilitation but significantly reduced rate-related fatigue (by 31 +/- 8%, mean +/- SEM, P < .05, in rabbit hearts; 46 +/- 5%, P < .01, in guinea pig hearts). Combined inhibition of adenosine deaminase (with erythro-9-[2-hydroxy-3-nonyl]-adenine hydrochloride, 5 mumol/L) and adenosine uptake (with dipyridamole, 1 mumol/L) increased fatigue in the absence of exogenous adenosine by 57 +/- 20% (P < .05).

CONCLUSIONS

We conclude that (1) exogenously administered adenosine increases AV nodal fatigue and reduces facilitation, without altering AV nodal recovery; (2) these changes cause rate-dependent AV nodal depression, which plays a role in adenosine's actions on experimental AVRT; and (3) endogenous adenosine receptor activation plays a role in physiological AV nodal fatigue. Adenosine's ability to terminate reentrant supraventricular tachycardia may be due, at least in part, to its ability to enhance the physiological conduction slowing that results from sustained increases in AV nodal activation rate.
Platelet activation during coronary angioplasty in humans.
Authors: Gasperetti C M , Gonias S L , Gimple L W , Powers E R
Published: June 2012

BACKGROUND

Previous studies have indicated that balloon angioplasty is associated with local platelet activation. In addition, different contrast media have different effects on thrombus formation during angioplasty in humans. We hypothesized that coronary angioplasty in humans is associated with activation of platelets to specific platelet agonists and that this activation may be differently modified by different angiographic contrast agents.

METHODS AND RESULTS

We studied 25 patients referred for angioplasty of the left anterior descending or circumflex coronary arteries. All patients were pretreated with aspirin and received heparin. Blood samples for assessment of platelet aggregation to serotonin, ADP, epinephrine, and collagen were obtained from the coronary sinus before any contrast injection, after initial diagnostic contrast injections, and after three balloon inflations. Patients were randomized to receive iopamidol, diatrizoate, or ioxaglate. Contrast alone was not associated with altered platelet aggregation. However, balloon angioplasty was consistently associated with increased platelet aggregation to serotonin but not to ADP, epinephrine, or collagen. These effects were similar with the three contrast agents studied except that the use of iopamidol was associated with increased platelet responsiveness to all concentrations of ADP after balloon dilation.

CONCLUSIONS

Coronary angioplasty in humans was associated with increased platelet aggregation in blood drawn from the coronary sinus. This effect was primarily seen when serotonin was used as an agonist.
Responsiveness to bradykinin in veins of hypercholesterolemic humans.
Authors: Bedarida G V , Bushell E , Haefeli W E , Blaschke T F , Hoffman B B
Published: June 2012

BACKGROUND

Hypercholesterolemia impairs endothelium-dependent dilation in arteries. We tested the hypothesis that hypercholesterolemia impairs endothelium-dependent vasodilation by an interaction between elevated plasma lipoproteins and a presumably normal endothelium using human veins in vivo; veins do not generally develop atherosclerosis and are appropriate for testing functional alterations.

METHODS AND RESULTS

Full dose-response curves were constructed in 13 hypercholesterolemic and 12 normocholesterolemic subjects by infusing bradykinin (0.25 to 508 ng/min) into hand veins preconstricted with the alpha-adrenergic agonist phenylephrine. The maximal relaxation induced by bradykinin was 80 +/- 38% in the controls and 103 +/- 40% in subjects with hypercholesterolemia (P = .08). Responsiveness to bradykinin was also determined after infusion of indomethacin (5.4 micrograms/min), a cyclooxygenase inhibitor, to block the contribution of prostaglandins; maximal responsiveness was greater in hypercholesterolemic subjects (112 +/- 41%) than in controls (81 +/- 31%) (P = .03). Hypercholesterolemic subjects were more sensitive to bradykinin, with an ED50 of 4.2 ng/min versus 10.9 ng/min in controls (P = .05); a similarly increased sensitivity was found in the presence of indomethacin. The response to a maximally effective dose of nitroglycerin was greater in hypercholesterolemic subjects (142 +/- 31%) versus 106 +/- 28% in controls (P = .007). In five hypercholesterolemic subjects, treated with lovastatin to normalize serum cholesterol concentrations, maximal responsiveness to bradykinin decreased from 103 +/- 52% to 80 +/- 28%.

CONCLUSIONS

These results demonstrate that hypercholesterolemia in humans does not impair endothelium-derived relaxing factor-mediated venodilation.
Intramural myocardial shortening in hypertensive left ventricular hypertrophy with normal pump function.
Authors: Palmon L C , Reichek N , Yeon S B , Clark N R , Brownson D , Hoffman E , Axel L
Published: June 2012

BACKGROUND

In hypertensive left ventricular hypertrophy (LVH), intrinsic myocardial systolic function may be normal or depressed. Magnetic resonance tagging can depict intramural myocardial shortening in vivo.

METHODS AND RESULTS

Tagged left ventricular magnetic resonance images were obtained in 30 hypertensive subjects with LVH (mean LV mass index, 142 +/- 41 g/m) and normal ejection fraction (mean, 64 +/- 9%) using spatial modulation of magnetization. In 26 subjects, circumferential myocardial shortening (%S) was compared with results obtained in 10 normal subjects at endocardium, midwall, and epicardium on up to 4 short-axis slices each. Similarly, in 10 subjects, midwall long-axis shortening at basal, midventricular, and apical sites was compared with results obtained in 12 normal volunteers. Circumferential %S was reduced in hypertensive subjects. Mean shortening was 29 +/- 6% at the endocardium in hypertensive subjects versus 44 +/- 6% in normal subjects (P = .0001); 20 +/- 6% at the midwall versus 30 +/- 6% (P = .0001); and 13 +/- 5% at the epicardium versus 21 +/- 5% (P = .0002). However, the transmural gradient in percent shortening from endocardium to epicardium in hypertensive subjects paralleled that in normal subjects. The normal base-to-apex gradient in circumferential %S was absent in LVH. In contrast to normal subjects, circumferential %S showed regional heterogeneity in hypertensive subjects, being maximal in the lateral wall and least in the inferior wall. Longitudinal shortening was also uniformly depressed in hypertensive subjects: 10 +/- 9% at the base versus 21 +/- 6% in normal subjects (P = .0001); 14 +/- 8% at the midventricle versus 18 +/- 3% (P = .03); and 14 +/- 8% at the apex versus 18 +/- 4% (P = .04).

CONCLUSIONS

In hypertensive LVH with normal pump function, intramural circumferential and longitudinal myocardial shortening are depressed.
Prediction of outcome after valve replacement for rheumatic mitral regurgitation in the era of chordal preservation.
Authors: Wisenbaugh T , Skudicky D , Sareli P
Published: June 2012

BACKGROUND

Noninvasive predictors of important outcomes after valve replacement for mitral regurgitation have not been examined in a rheumatic population (in whom the results of valve repair are suboptimal) in the era of chordal preservation. Timing of valve replacement thus remains a difficult question in rheumatic mitral regurgitation.

METHODS AND RESULTS

Of 278 patients followed after valve replacement, 66 had pure or predominant mitral regurgitation, and in 61 of these the etiology was rheumatic. The mean age was 24 years. After a mean follow-up of 24 +/- 10 months, the ability of preoperative clinical and echocardiographic data to predict outcome was assessed prospectively, and the possible impact of chordal preservation (n = 35) on survival and post-operative left ventricular function was examined retrospectively. There were no perioperative deaths. There were six postoperative deaths, all the result of heart failure and all related to left ventricular dysfunction. The mean probability of survival was .90 at 16 months. In a stepwise Cox proportional hazards regression analysis, the only independent predictor of postoperative death was preoperative end-systolic diameter. According to a logistic model, the probabilities of death (n = 6) and death or severe heart failure (n = 7) increased abruptly at a preoperative end-systolic diameter of 51 mm (probabilities, .23 and .31, respectively), and the accuracy of this cut point for predicting outcomes was 97% and 98%, respectively. Multiple linear regression analysis identified a large preoperative end-systolic diameter and the need to use tricuspid annuloplasty as significant independent predictors of postoperative fractional shortening; the use of chordal preservation (n = 35) was not a predictor of postoperative fractional shortening. A good outcome was predicted at a preoperative end-systolic diameter of 40 mm: probability of death or heart failure was .0001, and predicted mean postoperative fractional shortening was 0.27 after mitral valve replacement without tricuspid annuloplasty.

CONCLUSIONS

When preoperative end-systolic diameter is more than 50 mm, a poor postoperative outcome is predicted despite chordal preservation in relatively young patients with rheumatic mitral regurgitation, and alternative strategies should therefore be considered. When preoperative end-systolic diameter is 40 mm or less, an excellent outcome is predicted, and close observation without surgery would appear to be reasonable in the absence of symptoms.
Reconsideration of criteria for the Fontan operation. Influence of pulmonary artery size on postoperative hemodynamics of the Fontan operation.
Authors: Senzaki H , Isoda T , Ishizawa A , Hishi T
Published: June 2012

BACKGROUND

The outcome of the Fontan operation largely depends on patient selection because this procedure is a physiological correction. Among the several selection criteria for the Fontan operation, the importance of adequate size of the pulmonary artery remains controversial. To clarify whether or not pulmonary artery size is indispensable as one of the selection criteria for the Fontan operation, we considered the physiological importance of pulmonary artery size and investigated how pulmonary artery size influenced postoperative hemodynamics of the Fontan operation.

METHODS AND RESULTS

In congenital heart disease of decreasing pulmonary blood flow, 40 patients were examined for this analysis. Pulmonary artery indexes (cross-sectional area of the right and left pulmonary arteries divided by body surface area) were measured as the expression of pulmonary artery size, and the relations of pulmonary artery index (PAI) to pulmonary vascular resistance (Rp) and compliance (Cp) were studied. There was no significant correlation between PAI and Rp, whereas a significant correlation was found between PAI and Cp (r = .71, P = .001). Furthermore, Cp influenced postoperative hemodynamics of the Fontan operation by affecting peak central venous pressure and total impedance, which was the afterload to the ventricle. Impedance increased abruptly when PAI was less than approximately 100 mm2/m2.

CONCLUSIONS

The smaller pulmonary artery size is hemodynamically disadvantageous after the Fontan operation, with resultant rise in peak control venous pressure and increased afterload to the single ventricle.
Intracoronary ultrasound assessment of morphological and functional abnormalities associated with cardiac allograft vasculopathy.
Authors: Heroux A L , Silverman P , Costanzo M R , O'Sullivan E J , Johnson M R , Liao Y , McKiernan T L , Balhan J E , Leya F S , Mullen G M
Published: June 2012

BACKGROUND

The diffuse nature of cardiac allograft vasculopathy makes early detection of the disease by traditional noninvasive methods or coronary angiography difficult. The aim of this study was to determine if there is a relation between abnormalities in vessel wall morphology, as assessed by intracoronary ultrasound, and a decreased vasodilatory response to the endothelium-dependent vasodilator papaverine hydrochloride and if cardiac allograft vasculopathy detected by coronary angiography is associated with specific intracoronary ultrasound findings.

METHODS AND RESULTS

Twenty-three heart transplant recipients underwent 25 intracoronary ultrasound studies and 24 studies of coronary vasomotor tone 10 days to 8.3 years after surgery using a 20-mHz intracoronary ultrasound catheter. The studies were divided in two groups according to the presence (n = 7, group 1) or absence (n = 18, group 2) of angiographically evident cardiac allograft vasculopathy. Qualitative assessment of vessel wall morphology and quantitative analysis of the vasodilator response to the injection of papaverine hydrochloride into the coronary artery distal to the imaging site were performed off-line, and results for the two study groups were compared. A significantly higher percentage of patients with than without angiographic evidence of cardiac allograft vasculopathy had a three-interface vessel wall morphology by intracoronary ultrasound (100% versus 11%, P < .001). In two recipients who underwent two serial studies, the appearance of three interfaces in the vessel wall or a progressive thickening of the inner interface of the vessel wall occurred in conjunction with the appearance of angiographic cardiac allograft vasculopathy. The vasodilator response to papaverine was less in patients with than in those without angiographically evident cardiac allograft vasculopathy both in terms of absolute and relative increases in lumen diameter (+0.1 +/- 0.12 mm versus +0.3 +/- 0.17 mm, P < .05, and +5.1 +/- 5.3% versus +8.2 +/- 5.3%, P = NS) and lumen cross-sectional area (+0.5 +/- 0.6 mm2 versus +1.7 +/- 1.1 mm2, P < .02, and +7.1 +/- 8.8% versus 16.6 +/- 11.0%, P = .055), respectively.

CONCLUSIONS

Intracoronary ultrasound assessment of vessel wall morphology and evaluation of vascular response to endothelium-dependent vasodilators are useful techniques for detecting cardiac allograft vasculopathy.
Myocardial perfusion and ventricular function measurements during total coronary artery occlusion in humans. A comparison with rest and exercise radionuclide studies.
Authors: Borges-Neto S , Puma J , Jones R H , Sketch M H , Stack R , Hanson M W , Coleman R E
Published: June 2012

BACKGROUND

The purpose of this investigation was to compare the magnitude of change in myocardial perfusion and function during exercise with that obtained during total coronary artery occlusion. Radionuclide studies are widely used for the diagnosis and determination of prognosis in patients with suspected or known coronary artery disease. These studies are based on the premise that the relative deficit of coronary blood flow, which is induced by exercise and recognized as increased demand, relates to the jeopardy experienced by the decrease or sudden absolute interruption of coronary blood flow that is recognized as decreased supply and is associated with coronary stenosis or total coronary artery occlusion. The magnitude of exercise-induced perfusion and function abnormalities compared with those induced by total coronary artery occlusion in humans has not been previously reported.

METHODS AND RESULTS

We prospectively studied 20 patients with > or = 50% diameter stenosis documented by quantitative coronary angiography in at least one vessel. A same-day rest/exercise sestamibi myocardial function and perfusion study was performed within 24 hours before percutaneous transluminal coronary angioplasty. At 1 minute after balloon inflation, while the vessel was occluded, sestamibi was injected, and a myocardial perfusion and function study was performed. Perfusion defect size was greater during occlusion (28 +/- 3%) than during exercise (13 +/- 2%) (P < .01). Ejection fraction was greater during exercise (53 +/- 3%) compared with values measured during occlusion (41 +/- 2%) (P < .01).

CONCLUSIONS

Physiological abnormalities induced by coronary occlusion are greater than those that occur during exercise, thereby indicating that stress-induced ischemia may not reflect the total potential myocardium in jeopardy from a stenotic lesion, if sudden occlusion occurs.
Does external ultrasound accelerate thrombolysis? Results from a rabbit model.
Authors: Kornowski R , Meltzer R S , Chernine A , Vered Z , Battler A
Published: June 2012

BACKGROUND

Prior in vitro and in vivo studies have reported that external ultrasound accelerates thrombolysis at intensities too low to have a direct effect on clot dissolution in the absence of a thrombolytic agent. The present study was undertaken to examine the ultrasound effect on thrombolysis and reocclusion in a rabbit thrombosis model.

METHODS AND RESULTS

Blood clots were produced in a femoral artery segment with endothelial damage and distal stenosis. Recombinant tissue-type plasminogen activator (rTPA) was infused at 30 micrograms.kg-1.min-1 for 60 minutes. Femoral artery flow was measured every 5 minutes for 2 hours. Rabbits were randomized to four groups with continuous wave ultrasound on or off with or without intravenous injection of 17 mg/kg aspirin (+US/-US/+Asp/-Asp). Ultrasound frequency and intensity were 1 MHz and 6.3 W/cm2. In seven of eight and five of five rabbits given rTPA and -US/-Asp or -US/+Asp, respectively, reflow was observed, persisting to the end of the observation period. In five of nine and four of five rabbits given rTPA and +US/-Asp or +US/+Asp, reflow was achieved, but persistent reocclusion was subsequently observed in five of five and two of four of these rabbits, respectively. Overall, femoral artery patency was worse and reocclusion occurred more often when ultrasound was added to rTPA (P = .002 by nonparametric ANOVA). However, initial reflow occurred more rapidly with ultrasound exposure (21 +/- 10 and 33 +/- 6 minutes for the +US/+Asp and +US/-Asp groups, respectively) compared with without ultrasound (46 +/- 13 and 74 +/- 14 minutes for the -US/+Asp and -US/-Asp groups, respectively) (P = .03 by ANOVA).

CONCLUSIONS

Although time to initial reflow was shortened by ultrasound, it was associated with less reperfusion and more reocclusion in this model. A possible explanation for these results is ultrasound-induced platelet activation counterbalancing its thrombolysis-accelerating effect.
Coronary reperfusion enhances recovery of atrial natriuretic peptide secretion. Salvaging endocrine function in patients with acute right ventricular infarction.
Authors: Yasuda S , Nonogi H , Miyazaki S , Goto Y , Haze K
Published: June 2012

BACKGROUND

The heart has been demonstrated not only to be a pumping organ but also an endocrine organ secreting atrial natriuretic peptide (ANP). We hypothesized that myocardial ischemia may affect ANP secretion and that reperfusion therapy for acute myocardial infarction can preserve endocrine function of the heart.

METHODS AND RESULTS

Twenty patients with acute right ventricular infarction were examined who underwent reperfusion therapy on admission. These patients had proximal occlusion of the dominant right coronary artery involving the right atrial branches: 9 patients with successful reperfusion (SRP group) and the remaining 11 patients with unsuccessful reperfusion (URP group). Within 24 hours after the onset of infarction, a volume loading test was performed after reperfusion therapy with measurements for plasma ANP levels and hemodynamics. Before the volume loading test, the plasma ANP level and mean right atrial pressure were similar between these two groups. However, in the URP group, percent increase in ANP in response to volume loading was strikingly smaller (URP, 45 +/- 18% versus SRP, 133 +/- 25%; P < .01) despite similar percent increase in mean right atrial pressure (URP, 100 +/- 46% versus SRP, 86 +/- 23%). The peak ANP level occurred significantly later in the URP group (69 +/- 16 hours) than in the SRP group (28 +/- 9 hours, P < .001) after the onset of infarction.

CONCLUSIONS

The response of ANP release to volume loading is attenuated in patients with right ventricular infarction without coronary reperfusion. However, successful reperfusion induces a rapid recovery of cardiac endocrine function as well as its mechanical function. A sufficiently elevated plasma ANP level may be a useful predictor of hemodynamic improvement in patients with right ventricular infarction.