bluuebunny/crossref_metadata_2025 huggingface dataset:
A controlled trial of corticosteroids to prevent restenosis after coronary angioplasty. M-HEART Group.
Authors: Pepine C J , Hirshfeld J W , Macdonald R G , Henderson M A , Bass T A , Goldberg S , Savage M P , Vetrovec G , Cowley M , Taussig A S
Published: June 2011

A multicenter, double-blind, placebo-controlled trial was conducted to determine if corticosteroids influence the development of restenosis after successful percutaneous transluminal coronary angioplasty (PTCA). Either placebo or 1.0 g methylprednisolone (steroid) was infused intravenously 2-24 hours before planned PTCA in 915 patients. The PTCA patient success rate was 87% (mean) in the eight centers. There were no differences in clinical or angiographic baseline variables between the two groups. End-point analysis (angiographic restenosis, death, recurrent ischemia necessitating early restudy, and coronary artery bypass graft surgery) showed that there was no significant difference comparing placebo- with steroid-treated patients. Angiographic restudy showed the lesion restenosis rate to be 39% (120 of 307 lesions) after placebo and 40% (117 of 291) after steroid treatment (p = NS). We conclude that pulse steroid pretreatment does not influence the overall restenosis rate after successful PTCA.
Percutaneous coronary excimer laser angioplasty in patients with stable and unstable angina pectoris. Acute results and incidence of restenosis during 6-month follow-up.
Authors: Karsch K R , Haase K K , Voelker W , Baumbach A , Mauser M , Seipel L
Published: June 2011

A clinical study was conducted to evaluate the efficacy and safety of percutaneous coronary excimer laser angioplasty in 60 patients with coronary artery disease. Forty-nine patients had stable exertional angina, and 11 patients had unstable angina despite medical therapy. A novel 1.4-mm diameter catheter with 20 quartz fibers of 100-microns diameter each arranged concentrically around a central lumen suitable for a 0.014-in. flexible guide wire was coupled to an excimer laser. A commercial excimer laser emitting energy at a wavelength of 308 nm with a pulse duration of 60 nsec was used. The laser was operated at 20 Hz. Mean energy transmission was 30 +/- 5 mJ/mm2. In five of the 60 patients, laser angioplasty was not attempted. In 23 patients with laser ablation alone, percent stenosis decreased from 76 +/- 14% before to 27 +/- 17% after ablation and was 34 +/- 15% at the early follow-up angiogram. In 32 patients, additional balloon angioplasty was performed because of vessel closure after laser ablation in 11 and an insufficient qualitative result in 21 patients. Of the 11 patients with unstable angina, one patient died due to vessel closure 3 hours after intervention, and two patients developed a myocardial infarction. In 22 of 47 patients with late follow-up angiography, restenosis within the 6-month follow-up period occurred. Rate of restenosis was higher in patients treated with laser ablation and balloon angioplasty (16 of 28) than in patients treated with laser ablation alone (six of 19). These results suggest that coronary excimer laser angioplasty for ablation of obstructive lesions is feasible and safe in patients with stable angina. However, development of new catheter systems is necessary for an improved success rate.
Long-term impairment of endothelium-dependent relaxations to aggregating platelets after reperfusion injury in canine coronary arteries.
Authors: Pearson P J , Schaff H V , Vanhoutte P M
Published: June 2011

Experiments were designed and performed to determine whether endothelial function remained chronically impaired after coronary artery reperfusion. Canine left anterior descending coronary arteries were exposed to ischemia (60 minutes) followed by reperfusion (12 weeks). Rings (3-4 mm wide) of the reperfused artery and of normal left circumflex (control) coronary artery segments were suspended in organ chambers containing physiological saline solution (37 degrees C, gassed with 95% O2-5% CO2) for isometric force measurement. Endothelium-independent contractions to KCl or prostaglandin F2 alpha and endothelium-independent relaxations to nitric oxide or isoproterenol were comparable in control and chronically reperfused arteries. However, chronically reperfused coronary arteries exhibited impaired endothelium-dependent relaxations to aggregating platelets. In addition, the reperfused coronary arteries exhibited impaired endothelium-dependent relaxations to the platelet-derived compounds adenosine diphosphate, serotonin, and thrombin. However, the endothelium-dependent relaxations to acetylcholine were comparable between control and reperfused arteries. Thus, after 12 weeks of reperfusion, previously occluded coronary arteries exhibited a selective impairment of endothelium-dependent relaxation evoked by aggregating platelets. In vivo, this phenomenon could favor platelet adhesion, aggregation, and platelet-induced contraction of coronary smooth muscle and thus facilitate ischemic events such as vasospasm and coronary thrombosis.
Conjugation to antifibrin Fab' enhances fibrinolytic potency of single-chain urokinase plasminogen activator.
Authors: Bode C , Runge M S , Schönermark S , Eberle T , Newell J B , Kübler W , Haber E
Published: June 2011

Single-chain urokinase plasminogen activator (scu-PA) that had been modified with N-succinimidyl-3-(2-pyridyldithio)propionate was covalently linked by disulfide bonds to the Fab' of a monoclonal antibody specific for the beta-chain of fibrin (antibody 59D8). scu-PA-59D8 Fab' conjugate was separated from free scu-PA and two-chain urokinase coupled to 59D8 Fab' by two-step affinity chromatography. First, the reaction mixture was chromatographed on a column containing Sepharose linked to the peptide that had been used as immunogen for antibody 59D8; scu-PA-59D8 Fab' conjugate and unconjugated 59D8 Fab' were retained but not unconjugated scu-PA. Then, the eluate from the peptide-Sepharose column was chromatographed on a column containing Sepharose linked to benzamidine, which acts as a ligand for two-chain urokinase. The molecular weight of the scu-PA-59D8 Fab' conjugate was approximately 100 kDa when electrophoresed on a nonreducing sodium dodecylsulfate-polyacrylamide gel. Enzymatic assay after purification revealed that more than 97% of the scu-PA present in the conjugate retained the single-chain form. The Fab' portion of the conjugate functioned in a manner indistinguishable from that of native antibody 59D8. In an in vitro assay for lysis of fibrin monomer, the fibrinolytic potency of scu-PA-59D8 Fab' was 33-fold more than that of tissue plasminogen activator (p less than 0.001), 230-fold more than that of unconjugated scu-PA (p less than 0.0001), and 420-fold more than that of urokinase (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
Threshold concentrations of endothelin-1 potentiate contractions to norepinephrine and serotonin in human arteries. A new mechanism of vasospasm?
Authors: Yang Z H , Richard V , von Segesser L , Bauer E , Stulz P , Turina M , Lüscher T F
Published: June 2011

Endothelin-1 is an endothelium-derived vasoconstrictor peptide. Its circulating levels are below those known to evoke direct vascular effects. To study whether low concentrations of endothelin-1 potentiate the effects of other vasoconstrictor hormones, we suspended isolated human internal mammary and left anterior descending coronary artery rings in organ chambers for isometric tension recording. In mammary artery rings, the contractions to norepinephrine (3 x 10(-8) M) were potentiated by threshold (3 x 10(-10) M) and low concentrations (10(-9) M) of endothelin-1 (96 +/- 35% and 149 +/- 58% increase from control; p less than 0.01 and 0.001; n = 6). The inhibitor of endothelial nitric oxide formation L-NG-monomethyl arginine did not affect the potentiating effects of the peptide. The calcium antagonist darodipine (10(-7) M) prevented the potentiation of the response to norepinephrine evoked by endothelin-1. Similarly, contractions to serotonin (10(-7) or 3 x 10(-8) M) were amplified by endothelin-1 (3 x 10(-10) M) in the mammary (30 +/- 9%) and in the coronary arteries (59 +/- 25%). Endothelin-1 (10(-9) M) further potentiated the response (57 +/- 23% in mammary and 87 +/- 26% in coronary arteries; p less than 0.05; n = 7 and 3). The sensitivity of mammary arteries to calcium chloride was markedly enhanced in the presence of endothelin-1 (3 x 10(-10) M; concentration shift, eightfold; p less than 0.01; n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)
Premature escape beats. A model for triggered activity in the intact heart?
Authors: Vos M A , Gorgels A P , de Wit B , Drenth J P , van Deursen R T , Leunissen J D , Wellens H J
Published: June 2011

In conscious dogs with complete atrioventricular block, overdrive pacing of the idioventricular rhythm normally results in overdrive suppression (OS). Frequently, however, we observed another response to overdrive, that is, QRS complex or complexes with unexpectedly short coupling intervals followed by normal OS. We have named such a QRS complex a "premature escape beat" (PEB). Based on the response of PEBs to electrical stimulation, we postulate that PEBs are based on triggered activity resulting from delayed afterdepolarizations. This hypothesis was tested in 82 experiments by 1) stimulation under control conditions and in combination with 2) subtoxic and toxic amounts of ouabain 20-50 micrograms/kg, 3) lidocaine 3 mg/kg, and 4) doxorubicin 16-24 mg/m2. The stimulation protocol, which was repeated at random five to 10 times, consisted of 10 and 50 stimuli using interstimulus intervals of 200, 400, 600, and 800 msec. This protocol was not only performed during spontaneous idioventricular rhythm but also during a continuously paced rhythm with interstimulus intervals of 800 msec. It was found that 1) the chance to induce a PEB or PEBs increased and 2) their first postpacing interval significantly decreased using short or fast drives, or both. Ouabain increased significantly and in a dose-dependent manner 1) the ability to induce PEBs and 2) the number of PEBs per stimulation-train, and also shortened their first postpacing interval. Opposite effects were seen after lidocaine, doxorubicin, and continuous pacing as follows: 1) a lower incidence of PEBs and 2) lengthening of their first postpacing interval. These results support our hypothesis that PEBs are based on triggered activity resulting from delayed afterdepolarizations.
Mechanism of cardiac defibrillation in open-chest dogs with unipolar DC-coupled simultaneous activation and shock potential recordings.
Authors: Witkowski F X , Penkoske P A , Plonsey R
Published: June 2011

The automatic implantable cardioverter-defibrillator has been shown to dramatically improve survival. The future refinement of these devices requires a clear understanding of their mechanism of action. We performed the following study to test two hypotheses: 1) When defibrillation is successful, fibrillating activity must be annihilated in a critical mass of both ventricles; and 2) when defibrillation is unsuccessful, at least one area of the ventricular mass has been left fibrillating. Unipolar Ag/AgCl sintered electrodes were directly coupled from triangular arrays at 40 epicardial locations (total, 120 recording sites) that covered both right and left ventricular surfaces and were designed to measure the voltage gradient generated by the shock at each triangular array as well as the underlying myocardial electrical activity before and immediately after the shock. An algorithm was developed and tested that reliably scored whether a postshock activation was a continuation of the immediately previous fibrillating activity. This technique was applied to 203 defibrillation attempts in six open-chest dogs during electrically induced ventricular fibrillation. There were 139 successful defibrillation attempts and 64 unsuccessful attempts. Monophasic truncated exponential 10-msec defibrillation shocks (0.5-35 J) were delivered through an anodal patch on the right atrium and a cathodal patch on the left ventricular apex. In all cases of unsuccessful defibrillation, at least one ventricular site could be clearly identified that failed to be defibrillated. In cases of successful defibrillation two distinct patterns were observed: 1) complete annihilation of fibrillating activity at all sites or 2) nearly complete cessation of fibrillating activity with a single area of persistent fibrillation that subsequently self-extinguished within one to three activations. This single site in the second form of successful defibrillation was located in the region of minimum voltage gradient produced by the defibrillating waveform and was occasionally accompanied by dynamic encapsulation with refractory tissue as a result of a wavefront emanating from a region that had undergone successful defibrillation. These results support the hypothesis that a critical mass of myocardium must be affected for successful defibrillation and that unsuccessful defibrillation is always accompanied by residual fibrillating activity in at least one site. The results also demonstrate that the size of the critical mass required for successful defibrillation can be less than 100%.
Block of delayed rectifier potassium current, IK, by flecainide and E-4031 in cat ventricular myocytes.
Authors: Follmer C H , Colatsky T J
Published: June 2011

Block of the delayed rectifier potassium current, IK, by the class IC antiarrhythmic agent, flecainide, and by the novel selective class III antiarrhythmic agent, E-4031, were compared in isolated cat ventricular myocytes using the single suction-pipette, voltage-clamp technique. Flecainide (10 microM) markedly reduced IK elicited on depolarization steps to plateau voltages (+10 mV) and nearly completely blocked the "tail currents" elicited on repolarization to -40 mV (93 +/- 4% block at +40 mV, n = 3). E-4031 (1 microM) produced similar effects (96 +/- 3% block at +40 mV, n = 3). Slow voltage ramps from -100 to +40 mV confirmed inward rectifying properties of IK and showed that flecainide and E-4031 have no effects on the background potassium current, IK1. Thus, the results demonstrate that block of IK is a common feature of flecainide and E-4031. IK block by E-4031 most likely underlies the drug's potent class III antiarrhythmic properties. On the other hand, flecainide block of IK during an action potential would tend to prolong repolarization, but this effect may be obscured by concomitant block of plateau Na+ channels to produce little or no change in action potential duration, consistent with its class IC classification.
Detection of enterovirus RNA in myocardial biopsies from patients with myocarditis and cardiomyopathy using gene amplification by polymerase chain reaction.
Authors: Jin O , Sole M J , Butany J W , Chia W K , McLaughlin P R , Liu P , Liew C C
Published: June 2011

Recent molecular studies have suggested that viral myocarditis frequently underlies human congestive cardiomyopathy; however, only moderately sensitive and specific techniques were used. Polymerase chain reaction (PCR) gene amplification is a sensitive, specific technique ideally suited for the diagnosis of viral disease in small tissue samples where low copy numbers of the viral genome may be present. Using PCR and high stringency condition, we screened biopsies taken from 48 patients with clinically suspected myocarditis or dilated cardiomyopathy. Five patients demonstrated positive enteroviral signals by PCR; two of them had myocarditis by pathology, whereas the other three had changes consistent with cardiomyopathy. Four other patients had myocarditis diagnosed by pathology from 3 months to 1 year earlier but were now negative by both PCR and pathology. Both pathology and PCR were negative for active myocarditis in all other patients. Ventricular samples taken from left ventricular myectomy in four additional patients with hypertrophic cardiomyopathy, normal human ventricle samples, and uninfected monkey kidney cells were also negative by PCR. This study supports a link between viral infection and dilated cardiomyopathy in some patients. PCR gene amplification provides a new diagnostic approach to patients with suspected myocarditis.
Attenuated vasodilator responses to Mg2+ in young patients with borderline hypertension.
Authors: Fujita T , Ito Y , Ando K , Noda H , Ogata E
Published: June 2011

Limb vascular responses to magnesium (Mg2+) and potassium (K+) ions were studied in 19 young patients with borderline hypertension (BHT) and compared with those of 22 age-matched normotensive subjects (NT) by measuring the forearm blood flow response to intra-arterial infusion of magnesium sulfate and potassium chloride using venous occlusion plethysmography. Percent decrements of forearm vascular resistance with Mg2+ infusions were significantly less in BHT subjects than in NT (-37.2 +/- 4.2% versus -53.0 +/- 2.0%, p less than 0.05, during the infusion of 0.1 meq Mg2+/min, and -52.2 +/- 4.3% versus -65.6 +/- 1.5%, p less than 0.05, during the infusion of 0.2 meq Mg2+/min). Moreover, the relation of the magnitude of Mg2+ response to initial vascular resistance in six of 10 BHT subjects lies above the 95% confidence interval for predicted values calculated for response points in 11 NT subjects, suggesting attenuated vasodilator responses of Mg2+ in a significant proportion of BHT subjects. In contrast, the response points to K+ in eight of nine BHT subjects fall within the 95% confidence interval, suggesting normal vasodilator responses to K+ in the majority of BHT subjects. Furthermore, the effect of small increments in local serum calcium concentrations on Mg2(+)- and K(+)-induced vasodilation was studied in normal volunteers. Isosmolar CaCl2 solution infused into the same brachial artery at a rate of 0.09 meq/min severely blunted the vasodilating actions of Mg2+ (-30.1 +/- 6.5% versus -65.8 +/- 3.2%, p less than 0.01, during the infusion of 0.2 meq Mg2+/min) but did not affect those of K+ (-63.1 +/- 3.1% versus -55.9 +/- 3.8%, NS, during the infusion of 0.154 meq K+/min). It appears that Mg2(+)-induced vasodilation should be due to the antagonistic action of Mg2+ to calcium, but K(+)-induced vasodilation might not be directly related to calcium movement. Thus, these attenuated responses to Mg2+ but normal responses to K+ in BHT subjects may indicate an underlying defect in vascular Mg2+ metabolism, which ultimately may be related to the alterations in calcium handling by plasma membranes rather than to the abnormalities of membrane Na(+)-K+ pump activity.
Muscle blood flow during forearm exercise in patients with severe heart failure.
Authors: Arnold J M , Ribeiro J P , Colucci W S
Published: June 2011

Muscle fatigue is a prominent symptom in patients with chronic heart failure (CHF). To determine whether it results from an intrinsic abnormality of vasodilating capacity of the vasculature in exercising muscle, we studied local forearm blood flow (FBF) during exercise in 13 patients with severe CHF and in eight normal untrained subjects of similar age. Intermittent forearm static exercise was performed by squeezing a hand dynamometer for 5 seconds, three times per minute, for 5 minutes at 15%, 30%, and 45% of maximum voluntary contraction. FBF was measured by mercury-in-rubber strain gauge venous plethysmography at baseline before exercise and during the last 3 minutes of each exercise state. Exercise was repeated after 24 hours of intravenous administration of milrinone in the patients with CHF. FBF increased with forearm exercise in a reproducible manner during 24 hours in the normal subjects: rest, 2.54 +/- 0.23 (0 hours), 2.90 +/- 0.23, (24 hours); 15%, 7.25 +/- 0.92, 5.85 +/- 0.56; 30%, 9.20 +/- 1.08, 10.05 +/- 0.85; 45%, 14.62 +/- 1.64, 13.85 +/- 1.09 ml/100 ml/min; p = NS, 0 versus 24 hours. In patients with CHF, FBF was reduced at baseline compared with normal subjects (1.70 +/- 0.15 ml/100 ml/min, p less than 0.05), but no significant differences from normal subjects were observed during exercise (15%, 5.04 +/- 0.65; 30%, 7.64 +/- 0.99; 45%, 12.56 +/- 1.20 ml/100 ml/min). Peak exercise blood flow was correlated negatively with central venous pressure (r = -0.65, p less than 0.05) and positively with right ventricular ejection fraction (r = 0.59, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Isolated noncompaction of left ventricular myocardium. A study of eight cases.
Authors: Chin T K , Perloff J K , Williams R G , Jue K , Mohrmann R
Published: June 2011

Isolated noncompaction of left ventricular myocardium is a rare disorder of endomyocardial morphogenesis characterized by numerous, excessively prominent ventricular trabeculations and deep intertrabecular recesses. This study comprised eight cases, including three at necropsy. Ages ranged from 11 months to 22.5 years, with follow-up as long as 5 years. Gross morphological severity ranged from moderately abnormal ventricular trabeculations to profoundly abnormal, loosely compacted trabeculations. Echocardiographic images were diagnostic and corresponded to the morphological appearances at necropsy. The depths of the intertrabecular recesses were assessed by a quantitative echocardiographic X-to-Y ratio and were significantly greater than in normal control subjects (p less than 0.001). Clinical manifestations of the disorder included depressed left ventricular systolic function in five patients, ventricular arrhythmias in five, systemic embolization in three, distinctive facial dysmorphism in three, and familial recurrence in four patients. We conclude that isolated noncompaction of left ventricular myocardium is a rare if not unique disorder with characteristic morphological features that can be identified by two-dimensional echocardiography. The incidence of cardiovascular complications is high. The disorder may be associated with facial dysmorphism and familial recurrence.
Does reperfusion extend necrosis? A study in a single territory of myocardial ischemia--half reperfused and half not reperfused.
Authors: Ganz W , Watanabe I , Kanamasa K , Yano J , Han D S , Fishbein M C
Published: June 2011

The purpose of this study was to confirm or disprove the existence of reperfusion-induced extension of necrosis. To avoid the effect of the variability of collateral circulation when groups of dogs are compared, we compared the effect of reperfusion and nonreperfusion on myocardial necrosis in a single ischemic territory, half of which was reperfused and half of which was not. The left anterior descending coronary artery (LAD) territory between its last diagonal branch and the apex was studied because it was found to have uniform collateral blood flow. In 20 dogs, the LAD was occluded for 90-240 minutes to produce necrosis of different degrees of transmurality. Before release of this occlusion, the LAD was occluded distally halfway to the apex to keep the distal half nonreperfused. After 5 minutes of proximal reperfusion. Monastral blue dye was injected into the left atrium for demarcation of the reperfused region, and the heart was arrested, excised, cut parallel to the LAD, and placed into triphenyl tetrazolium chloride (TTC) solution for delineation of the region of necrosis. The validity of TTC staining under the conditions of this study was confirmed by light and electron microscopy. The transmurality of necrosis, measured within 1 or 0.5 cm on either side of the boundary, ranged from 30% to 88% of wall thickness and was not different in the reperfused compared with the nonreperfused region (paired t test). Reperfusion did not advance the epicardial edge of necrosis compared with the nonreperfused region. In conclusion, at 5 minutes after reperfusion, comparison of necrosis in the reperfused and nonreperfused halves of a single ischemic territory could not demonstrate an extension of necrosis by reperfusion.
Observations on electrode-tissue interface temperature and effect on electrical impedance during radiofrequency ablation of ventricular myocardium.
Authors: Haines D E , Verow A F
Published: June 2011

The purpose of this study was to correlate changes in electrical impedance with the electrode-tissue interface temperature and to characterize the associated events occurring at the catheter tip electrode. In a canine model, lesions were created in vitro (n = 49) and in vivo (n = 31) and radiofrequency power settings were varied. Electrode-tissue interface temperature, delivered current, and voltage were recorded, and impedance was calculated. A sudden rise in electrical impedance was seen in only two of 17 ablations in vitro and in one of 16 ablations in vivo with a peak electrode-tissue interface temperature of less than 100 degrees C compared with 29 of 32 ablations in vitro (p = 0.0001) and 12 of 15 ablations in vivo with a temperature of more than 100 degrees C (p = 0.0001). This phenomenon was associated with the observation of boiling and popping at the tip in in vitro preparations and tissue avulsion and thrombus formation on the catheter tip in in vivo studies. The lesion size was directly proportional to the peak temperature for all ablations but not to the peak power, current, or voltage during radiofrequency catheter ablation in the heart. Maintaining electrode-tissue interface temperature at less than 100 degrees C during radiofrequency catheter ablation in the heart may avoid the complications associated with the sudden rise in electrical impedance.
Incidence and consequences of periprocedural occlusion. The 1985-1986 National Heart, Lung, and Blood Institute Percutaneous Transluminal Coronary Angioplasty Registry.
Authors: Detre K M , Holmes D R , Holubkov R , Cowley M J , Bourassa M G , Faxon D P , Dorros G R , Bentivoglio L G , Kent K M , Myler R K
Published: June 2011

Of 1,801 patients in the 1985-1986 Percutaneous Transluminal Coronary Angioplasty (PTCA) Registry, 122 (6.8%) had periprocedural occlusion (4.9% in the catheterization laboratory, 1.9% outside the laboratory). Baseline patient factors independently associated with increased occlusion rates included triple-vessel disease, high risk status for surgery, and acute coronary insufficiency. Lesion characteristics showing significant positive association included severe stenosis before PTCA, diffuse or multiple discrete morphology, thrombus, and collateral flow from the lesion. Intimal tear and dissection were also very strongly associated with occlusion. Sixty patients (49%) had a transient occlusion that was reopened with PTCA, 43 (35%) were not redilated and managed with bypass surgery, and 19 (16%) were not redilated and managed medically. In-hospital mortality was 5% in each of these treatment groups, compared with 1% in occlusion-free patients. In-hospital infarction rates ranged from 27% in patients with transient occlusion to 56% in the patients managed with surgery, compared with 2% in patients without occlusion. During 2 years of follow-up, somewhat increased mortality continued in patients with occlusion, whereas follow-up infarction rates were comparable for all patients regardless of occlusion. Patients with an occlusion that was reopened or managed medically had increased rates of surgery during follow-up. Rates of repeat PTCA were comparable (about 23% by 2 years) in patients with transient occlusion and those without occlusion. Occlusion remains a serious complication of angioplasty and is associated most strongly with major events and surgical procedures that occur during the in-hospital period.
Double-umbrella closure of atrial defects. Initial clinical applications.
Authors: Rome J J , Keane J F , Perry S B , Spevak P J , Lock J E
Published: June 2011

Forty patients were catheterized for closure of atrial septal defects with the Rashkind patent ductus arteriosus umbrella device, a modified Rashkind umbrella device, and the newly designed Lock Clamshell Occluder. Patients weighed 8 kg or more (a requirement for transvenous access with the 11F delivery sheath) and had defects suitable for closure based on two-dimensional echocardiography. The new device was at least 1.6 times the diameter of the atrial septal defect as determined by balloon sizing at catheterization. Patients were followed up by telephone, clinical examination, and echocardiography at 6 months. We attempted closure in 34 patients, with atrial septal defects ranging in diameter from 3 to 22 mm; device sizes ranged from 17 to 33 mm. Initial device position immediately after release was correct in all patients. A cerebral embolus occurred in one elderly patient before device placement--the patient died 1 week later. Two instances of early device embolization occurred, and devices were retrieved by catheter without complication. Follow-up of 31 patients discharged with devices in place, for a total of 31 patient-years, has yielded no umbrella-related complications. Adequate imaging studies in 19 patients 6.5 months after device placement revealed no atrial shunt in 12; residual flow through separate, previously unrecognized atrial septal defects occurred in two; and small residual leaks (less than 3 mm) around devices were present in five patients. This initial success indicates that double-umbrella closure of atrial septal defects will aid in the treatment of intracardiac defects.
Early diagnosis of acute myocardial infarction based on assay for subforms of creatine kinase-MB.
Authors: Puleo P R , Guadagno P A , Roberts R , Scheel M V , Marian A J , Churchill D , Perryman M B
Published: June 2011

Thrombolytic therapy for patients with acute myocardial infarction (AMI) has produced the need for an accurate early diagnostic marker. We previously developed and assessed an assay for the creatine kinase (CK)-MB subforms; assay time is 25 minutes. Plasma MB2 (tissue subform) activity, MB1 (plasma-modified subform) activity, and MB2/MB1 ratio in 56 healthy individuals were 0.61 +/- 0.33 units/l, 0.63 +/- 0.33 units/l, and 0.94 +/- 0.39, respectively. Only one individual had both an MB2 activity greater than 1.0 units/l and an MB2/MB1 ratio of more than 1.5. Similar results were obtained in 50 hospitalized patients without cardiac disease; two of these patients had both an MB2 activity and an MB2/MB1 ratio greater than the cutoff values. Among 49 patients with AMI, MB2 activity and the MB2/MB1 ratio began to increase 2 hours after AMI; the ratio reached a plateau of 3.1 by 4-6 hours. The first available plasma sample was abnormal by the subform assay in 67% of patients and by a conventional MB assay in 27% of patients. Assay sensitivities in samples collected at 2-4, 4-6, and 6-8 hours after AMI were 59%, 92%, and 100% for the subform assay and 23%, 50%, and 71% for the conventional assay (p less than 0.03 versus subform assay at each time interval). False-negative results were obtained by the subform and conventional assays in 15 and 45 samples at a mean of 2.3 and 5.8 hours, respectively. Subform assay provides rapid and reliable diagnosis of AMI within 4-6 hours after the onset of symptoms, which is 6 hours before conventional CK-MB assays are accurate.
An evaluation of right and left ventricular function after anatomical correction and intra-atrial repair operations for complete transposition of the great arteries.
Authors: Martin R P , Qureshi S A , Ettedgui J A , Baker E J , O'Brien B J , Deverall P B , Yates A K , Maisey M N , Radley-Smith R , Tynan M
Published: June 2011

Anatomical correction of complete transposition of the great arteries has the potential advantage over intra-atrial repair in that the left ventricle becomes the systemic pump. To investigate the importance of this, we evaluated right and left ventricular function in 21 patients after anatomical correction and in 21 patients after Mustard or Senning operations. First-pass and equilibrium-gated radionuclide angiography were used to measure right and left ventricular ejection fractions between 17 and 78 (mean, 47) months after anatomical correction and between 3 and 187 (mean, 67) months after intra-atrial repair. The mean age of the patient groups at the time of study was 52 and 84 months, respectively. The right ventricular ejection fraction ranged from 35% to 78% (mean, 58%) in patients after anatomical correction and from 27% to 68% (mean, 51%) after intra-atrial repair (p = 0.066). The left ventricular ejection fraction ranged from 39% to 74% (mean, 58%) after anatomical correction and from 35% to 74% (mean, 58%) after intra-atrial repair (p = 0.86). The mean right and left ventricular ejection fractions of both groups were significantly lower than those of normal children. Individuals with systemic ventricular dysfunction were identified after both types of operations; however, symptomatic dysfunction occurred only after intra-atrial repair (p = 0.24).
Modification of human atrioventricular nodal function by selective atrioventricular nodal artery catheterization.
Authors: Wang P J , Sosa-Suarez G , Friedman P L
Published: June 2011

The hypothesis that human atrioventricular (AV) nodal function can be modulated selectively with a new technique of AV nodal artery catheterization was tested in eight subjects referred for diagnostic cardiac catheterization or electrophysiological studies. Three patients had no history of arrhythmias. Three patients had supraventricular tachycardia (SVT) due to reentry confined to the AV node (AVNRT). One patient had SVT due to reentry over a concealed AV bypass tract (AVRT-CBT), and one patient had nonsustained ventricular tachycardia. In each subject, sinus cycle length, AH interval, HV interval, AV nodal effective refractory period (AVN-ERP), and Wenckebach paced cycle length were measured in a control state. A flexible infusion catheter was then positioned selectively in the AV nodal artery of each subject. Through this catheter, a constant infusion of 0.1 mg/min procainamide at a flow rate of 0.125 ml/min (n = 1) or 50 micrograms/min acetylcholine at a flow rate of 0.25 ml/min (n = 4) was administered. Electrophysiological parameters were determined again during selective AV nodal artery drug infusion and during infusion of saline at identical rates. Two subjects developed transient AV nodal block during selective AV nodal catheterization alone and did not receive an infusion of drug or saline. A stable position of the AV nodal artery catheter could not be achieved in one other subject, who also received no drug or saline. In the other five subjects, drug infusion caused an increase in AVN-ERP from a control value of 312 +/- 52 msec to a value of 543 +/- 228 msec (p less than 0.05) and an increase in Wenckebach paced cycle length from a control value of 360 +/- 47 msec to a value of 572 +/- 217 msec (p less than 0.05). These parameters were unchanged from control during selective saline infusion. In two patients with AVNRT, drug infusion abolished SVT by causing complete blockade of ventriculoatrial conduction as well as lengthening of anterograde AVN-ERP. In the patient with AVRT-CBT, drug infusion abolished SVT by preventing repetitive anterograde AV conduction. Saline had no effect on SVT inducibility. Selective AV nodal artery catheterization enables AV nodal function to be modulated exclusively. Delivery of ablative agents to the AV node by this technique may be useful in patients with refractory SVT.
Spontaneous variability in ventricular ectopic activity during chronic antiarrhythmic therapy.
Authors: Anderson J L , Anastasiou-Nana M I , Menlove R L , Moreno F L , Nanas J N , Barker A H
Published: June 2011

Previous determinations of variability in frequency of ventricular arrhythmias have been based on repeated recordings obtained in the absence of therapy. We evaluate variability during "effective" treatment with antiarrhythmic drugs. Variability in the percent suppression of premature ventricular complexes (PVCs) was determined in 55 patients with chronic arrhythmias who underwent multiple ambulatory electrocardiographic recordings during evaluation of chronic therapy with antiarrhythmic drugs initially determined to be effective, which was defined as 70% or more reduction in total PVC frequency or 90% or more reduction in repetitive forms. During chronic therapy, total PVCs were suppressed by 92%, averaged after a logarithmic transformation step, and repetitive beats were suppressed by 88%. Variability in suppression was substantial. The one-sided 95% confidence intervals required a fall in suppression of total PVCs to 40% or less to exceed limits of spontaneous variability and of repetitive PVCs to 66% or less. Suppression declined at least once during therapy to less than 60% for total PVCs in 24 of 55 patients (44%) and to less than 80% for repetitive PVCs in 13 of 33 patients (39%); nine patients (16%) showed increases in PVC frequency at least once to levels above pretreatment baseline. Seven subgroups were analyzed for their effects on variability and loss of suppression: age, gender, disease etiology, cardiac function, baseline PVC frequency, use of beta-blockers, and class of antiarrhythmic drug. Differences in confidence bounds and loss of suppression were found to be determined in a complex way by subgroup differences in variability and in initial levels of PVC suppression. Variability was greater for patient subgroups with greater PVC frequency, beta-blocker therapy, and non-coronary artery disease. However, clinical loss of suppression was more common only in more elderly patients and those with worse cardiac function. In summary, substantial variability in arrhythmia frequency occurs during effective antiarrhythmic therapy, and the 95% confidence limits of spontaneous variability are broad and determined in a complex way. Careful consideration should be given before concluding on the basis of a single Holter test that changes (increases) in arrhythmia frequency, especially in certain subgroups, are caused by treatment failure.
A comparison of the pathological spectrum of hypertensive, diabetic, and hypertensive-diabetic heart disease.
Authors: van Hoeven K H , Factor S M
Published: June 2011

The hearts obtained at autopsy of 67 patients with hypertension, diabetes mellitus, or both were examined microscopically and histochemically, and the amount of fibrosis was determined. Significant differences in heart weight, interstitial fibrosis, replacement fibrosis, and perivascular fibrosis were found among the groups. The mean heart weight of the hypertensive-diabetic patients was significantly greater than that of the hypertensive patients and the diabetic patients. The amount of microscopic fibrosis increased between the groups, the lowest in hypertensive hearts, midrange in diabetic hearts, and highest in hypertensive-diabetic hearts. Total fibrosis correlated with heart weight among diabetic and hypertensive-diabetic patients and was significantly greater among patients with congestive heart failure, most of whom had histories of both hypertension and diabetes. The microscopic grade of fibrosis correlated significantly (p less than 0.01) with a quantitative, histochemical determination of the amount of collagen per milligram of total noncollagenous protein in the heart tissue. Myocardial fibrosis may contribute to the diastolic dysfunction typical of hypertensive-diabetic cardiomyopathy, in which congestive heart failure is a common sequela. The importance of hypertension in the pathogenesis of severe diabetic heart disease is discussed.
Baroreflex control of muscle sympathetic nerve activity in borderline hypertension.
Authors: Rea R F , Hamdan M
Published: June 2011

Patients with borderline hypertension have exaggerated vascular responses to orthostatic stress produced by tilt or lower body negative pressure (LBNP). It has been suggested that 1) in the supine position, these patients have augmented activity of cardiopulmonary baroreceptors that exerts an increased restraint on sympathetic vasoconstrictor tone; 2) withdrawal of this augmented inhibitory baroreceptor activity during orthostatic stress elicits augmented reflex sympathetic vasoconstrictor outflow; and 3) augmented cardiopulmonary baroreceptor activity may be secondary to impaired arterial baroreflex mechanisms. To test these hypotheses, we recorded muscle sympathetic nerve activity from the peroneal nerve in seven borderline hypertensive subjects and seven age-, sex-, and weight-matched normotensive subjects during three levels of nonhypotensive LBNP and infusions of phenylephrine and nitroprusside. During LBNP, reductions of central venous pressure were similar in borderline hypertensive and normotensive subjects, and arterial pressure and heart rate values were unchanged. Increases of sympathetic nerve activity, however, were significantly greater in borderline hypertensive than in normotensive subjects at each level of LBNP, indicating an augmented gain of the cardiopulmonary baroreflex. To determine whether this augmentation is related to impairment of arterial baroreflexes, we measured changes of sympathetic nerve activity during increases and decreases of arterial pressure produced with infusions of intravenous phenylephrine and nitroprusside. Central venous pressure was held at control levels by LBNP during phenylephrine and saline infusion during nitroprusside. Changes of sympathetic nerve activity during alterations of arterial pressure were similar in borderline hypertensive and normotensive subjects. These data show that cardiopulmonary baroreflex control of SNA is augmented in borderline hypertensive subjects and that this augmentation does not result from an attenuation of the arterial baroreflex.
Altered cardiovascular and neurohumoral responses to head-up tilt after heart-lung transplantation.
Authors: Banner N R , Williams T D , Patel N , Chalmers J , Lightman S L , Yacoub M H
Published: June 2011

Heart-lung transplantation results in afferent and efferent denervation of the transplanted organs including interruption of the central connections from the low-pressure receptors in the atria and pulmonary veins. We investigated whether the cardiovascular and neurohumoral responses to the postural stimulus of head-up tilt were affected after transplantation. Responses in eight heart-lung transplant recipients were studied and compared with those in eight normal subjects matched for age and sex during passive head-up tilt at 45 degrees for 1 hour. The transplant group had a higher initial heart rate (99 +/- 2 versus 68 +/- 2 beats/min, p less than 0.001) and diastolic blood pressure (88 +/- 5 versus 76 +/- 2 mm Hg, p less than 0.05) than did the control group. The increases in heart rate and diastolic blood pressure during head-up tilt were similar in the two groups. Systolic blood pressure remained unchanged. The decrease in cardiac output (30% versus 18%, p less than 0.05) and the increase in systemic vascular resistance (52% versus 28%, p less than 0.05) were greater in the transplant group. Baseline levels of norepinephrine, epinephrine, vasopressin, and plasma renin activity were similar in the two groups. Atrial natriuretic peptide concentrations were higher in the transplant group (26 +/- 3.8 versus 9.7 +/- 1.6 pmol/l, p less than 0.001). During head-up tilt, plasma norepinephrine levels increased to a greater extent in the transplant group than in the control group (83% versus 53%, p less than 0.01), indicating an increased sympathetic response. In contrast, plasma renin activity increased significantly in the control group but not in the transplant group.(ABSTRACT TRUNCATED AT 250 WORDS)
Morphological and electrophysiological correlates of atrioventricular nodal response to increased vagal activity.
Authors: Imaizumi S , Mazgalev T , Dreifus L S , Michelson E L , Miyagawa A , Bharati S , Lev M
Published: June 2011

The mechanisms responsible for slowing cardiac impulse conduction through the atrioventricular (AV) node are not well understood but include anatomical architecture, presence of cells with diverse electrophysiological characteristics, and modulation by autonomic nervous system. The present study was designed to determine the site of vagally induced slowing of conduction through the AV node. We attempted to correlate the electrophysiological response of AV nodal cells to postganglionic vagal stimulation applied in different regions of the node with the morphological findings and patterns of acetylcholinesterase-positive staining of nodal tissue. This multifaceted approach revealed that vagal stimulation produced localized hyperpolarization of the cells from the N region of the AV node, which correlated with the strong acetylcholinesterase positive staining of the central nodal area. In contrast, the density of the acetylcholinesterase staining decreased toward both the AN and His bundle regions, whereas vagal stimulation had a negligible effect on the cells from these regions. These results suggest that vagal-induced depression of AV nodal conduction is produced by release of acetylcholine predominantly around the midnodal region and the depressive action of acetylcholine is concentrated on the cells occupying the same region (i.e., the N cells). Thus, there appears to be a close juxtaposition of nerve elements and effector cells in the midnodal region of the AV node. This unique combination of available neuromediator and responding cells with hyperpolarization and depressed action potential determines the midnodal region as the focus of vagal effect on AV nodal conduction.
Assessment of mitral regurgitation by biplane transesophageal color Doppler flow mapping.
Authors: Yoshida K , Yoshikawa J , Yamaura Y , Hozumi T , Akasaka T , Fukaya T
Published: June 2011

To test the role of recently developed biplane transesophageal color Doppler echocardiography in the assessment of severity of mitral regurgitation, we examined 51 patients undergoing cardiac catheterization and left ventriculography. Transesophageal color Doppler flow imaging detected mitral regurgitation in all 32 patients proved to have this lesion. In 10 of 16 patients without mitral regurgitation by angiography, mitral regurgitation signals were detected by transesophageal color Doppler flow imaging. Thus, the sensitivity and specificity of transesophageal color Doppler echocardiography for the detection of mitral regurgitation were 100% and 38%, respectively. There was some correlation between the regurgitant jet area from the longitudinal plane and angiographic grading. An improved angiographic correlation was achieved with the regurgitant jet area from the transverse plane. The best correlation with angiography was obtained when the maximum regurgitant jet area from two planes (the greater of the two measurements, each from a different plane) was considered. There was a significant difference in the maximum regurgitant jet area between none and mild (p less than 0.01), mild and moderate (p less than 0.001), and moderate and severe (p less than 0.01) mitral regurgitation. The maximum regurgitant jet area of less than 1.5 cm2 predicted the angiographic grading as none with a sensitivity and specificity of 88% and 94%, respectively. The maximum regurgitant jet of between 1.5 and 4 cm2 predicted the angiographic grading as mild with a sensitivity and specificity of 82% and 95%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)