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Background: The success of pulmonary vein isolation (PVI) is reduced in persistent AF (PsAF) compared to paroxysmal AF. Adjunctive ablation strategies have failed to show consistent incremental benefit over PVI alone in randomized studies. The left atrial posterior wall is a potential source of non-PV triggers and atrial substrate which may promote the initiation and maintenance of PsAF. Adding posterior wall isolation (PWI) to PVI had shown conflicting outcomes, with earlier studies confounded by methodological limitations., Objectives: To determine whether combining PWI with PVI significantly improves freedom from AF recurrence, compared to PVI alone, in patients with PsAF., Methods: This is a multi-center, prospective, international randomized clinical trial. 338 patients with symptomatic PsAF refractory to anti-arrhythmic therapy (AAD) will be randomized to either PVI alone or PVI with PWI in a 1:1 ratio. PVI involves wide antral circumferential pulmonary vein (PV) isolation, utilizing contact force sensing ablation catheters. PWI involves the creation of a floor line connecting the inferior aspect of the PVs, and a roof line connecting the superior aspect of the PVs. Follow up is for a minimum of 12 months with rhythm monitoring via implantable cardiac device and/or loop monitor, or frequent intermittent monitoring with an ECG device. The primary outcome is freedom from any documented atrial arrhythmia of > 30 seconds off AAD at 12 months, after a single ablation procedure., Conclusions: This randomized study aims to determine the success and safety of adjunctive PWI to PVI in patients with persistent AF., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: A pilot study using a novel high-sensitivity cardiac troponin I (hs-cTnI) assay suggested that cTnI might be released into blood during exercise-induced myocardial ischemia. We investigated the potential clinical value of this signal., Methods: We included 819 patients with suspected exercise-induced myocardial ischemia referred for rest/bicycle myocardial perfusion single-photon emission computed tomography. The treating cardiologist used all available clinical information to quantify clinical judgment regarding the presence of myocardial ischemia using a visual analog scale twice: prior and after stress testing. High-sensitivity cTnI measurements were obtained before, immediately after peak stress, and 2 hours after stress testing in a blinded manner. Myocardial ischemia was adjudicated using perfusion single-photon emission computed tomography and coronary angiography findings., Results: Exercise-induced myocardial ischemia was detected in 278 (34%) patients. High-sensitivity cTnI levels were significantly higher at all time points in patients with myocardial ischemia as compared with those without (P < .001 for all). Combining clinical judgment prior exercise testing with baseline hs-cTnI levels increased diagnostic accuracy as quantified by the area under the receiver operating characteristics curve (AUC) from 0.672 to 0.757 (P < .001). Combining clinical judgment after exercise testing (AUC 0.704) with baseline or poststress hs-cTnI levels also increased the diagnostic accuracy (AUC 0.761-0.771, P < .001 for all). In contrast, exercise-induced changes in hs-cTnI during exercise did not seem useful, as they were small and similar in patients with or without myocardial ischemia., Conclusions: High-sensitivity cTnI concentrations at rest and after exercise, but not its exercise-induced changes, provide substantial incremental value to clinical judgment including exercise electrocardiography regarding the presence of myocardial ischemia., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Thirty-four patients with acute myocardial infarction (mean age 55 years) who received intracoronary streptokinase for coronary thrombosis were followed for a mean of 9.4 months (longest 25 months) following the procedure of percutaneous transluminal coronary recanalization (PTCR). Twelve patients had undergone coronary artery bypass graft surgery (CABG), one had percutaneous transluminal coronary angioplasty (PTCA), and 21 received medical therapy. Among patients having CABG and PTCA, nearly 70% no longer had chest pain or reinfarction, and 62% were in New York functional class I status; there were no deaths, and there was only one reinfarction, in a patient who had graft closure. In contrast, 43% of medically treated patients had chest pain or reinfarction or had died on follow-up; only 32% of survivors were in class I functional status. Further, 71% of medically treated patients who were receiving warfarin had no chest pain and on reinfarction, whereas the majority (56%) of patients who did not receive either warfarin or antiplatelet agents either had chest pain or reinfarction or died. The importance of CABG/PTCA and anticoagulant therapy is stressed to prevent recurrent ischemia, reinfarction, and reocclusion following successful reperfusion by means of PTCR in acute myocardial infarction.

Few data are available regarding the effects of calcium blockade upon exercise tolerance in patients with stable effort angina due to coronary artery disease (CAD). Therefore we compared the effects of the calcium blocking agent, diltiazem (D), to placebo (P) in 12 patients with chronic effort angina and catheterization documented fixed CAD. The 8-week total protocol consisted of a 1-week baseline period followed by the double-blind randomized crossover alternate 1-week administration of P and D in doses of 120, 180, and 240 mg. Maximal exercise tests (MET) were performed at the end of each 1-week period, while rest radionuclide ventriculography (RVG) was obtained during 240 mg D and corresponding crossover P. Resting heart rate decreased from baseline and initial P at D doses of 60 and 240 mg, but not from P during crossover period. No changes were observed at any dose of D either at rest or during MET in systolic blood pressure or rate . pressure double product. D at 240 mg, but not lower doses, increased MET duration (437 vs 490 seconds, p less than 0.01) and time to angina (383 vs 441 seconds, p less than 0.01). Ejection fraction by RVG was greater with D than P (0.54 vs 0.50, p less than 0.05). Thus these data indicate that calcium blockade with diltiazem provides antianginal efficacy by reducing myocardial oxygen demand, and increases exercise tolerance without depression of myocardial performance in effort angina patients with fixed chronic CAD.

To evaluate whether long-term administration of the oral vasodilator, prazosin, in the ambulatory therapy of chronic refractory congestive heart failure (CHF) results in gradual attentuation of its marked salutary peripheral circulatory relaxing actions, 16 coronary heart failure patients receiving chronic prazosin, 16 mg daily, were assessed for the development of vasodilator tolerance for 12 months. In six of these patients such tolerance was documented after 7 months which was readily surmountable, thereby allowing continuation of effective chronic prazosin therapy. Each of the six tolerance patients underwent four forearm plethysmography studies: prior to chronic prazosin (study I; 4.0 mg study dose), after 7 months prazosin (study II; 4.0 mg), repeated following 1 additional week on higher effective prazosin dose of 32 mg daily (study III; 8.4 mg), and following 2 weeks of prazosin withdrawal (study IV; 4.0 mg). The prazosin study dose increased forearm blood flow, decreased forearm vascular resistance and venous tone in studies I, III, and IV; these variables were unchanged by prazosin in study II. Despite vasodilator tolerance to the initial daily dosage at 7 months (study II), symptomatic effectiveness and improved cardiac performance were sustained throughout the entire 12 months of chronic prazosin therapy by increasing dosage (study III) and brief interruption of the vasodilator (study IV) (NYHA class IV pre-prazosin symptoms improved to class 2.7 at 3 months, class 2.4 at 6 months, and class 2.5 at 12 months chronic prazosin). This study showed that prazosin vasodilator tolerance occurred in approximately one third of CHF patients after several months of chronic prazosin therapy. More importantly, however, the present investigation demonstrated that chronic prazosin symptomatic efficacy can be maintained in such CHF patients by overcoming tolerance with higher effective prazosin dosage or brief prazosin discontinuation.

The efficacy and safety of intravenous loading of mexiletine was compared to lidocaine in patients with ventricular premature depolarizations (VPDs). Seventeen men and five women, average age 63 years, completed this randomized parallel study. Twelve patients received mexiletine intravenously at (5 to 10 mg/min) until greater than or equal to 95% VPD suppression was achieved or a total of 450 mg of drug was given. The average loading dose of mexiletine was 4.4 mg/kg, at an infusion rate of 0.1 mg/kg/min. Ten patients received lidocaine (1 mg/kg) given over 3 minutes, with a second similar bolus given if after 10 minutes greater than or equal to 95% VPD suppression was not achieved. Total VPDs were determined for the 60 minutes before drug administration, during drug infusion, and 60 minutes thereafter. Eleven of 12 (92%) patients receiving mexiletine were full responders (greater than or equal to 95% suppression) and one was a partial responder (greater than or equal to 75% greater than or equal to 95% suppression). Five of 10 lidocaine patients (50%) were full responders, three (30%) were partial responders, and two failed to respond. At peak suppression, mexiletine reduced mean VPD from 37 +/- 33/5 minutes (mean +/- S.D.) to 0.8 +/- 0.9/5 minutes (p less than 0.01) and lidocaine decreased mean VPDs from 28 +/- 47/5 minutes to 4.7 +/- 2.2/5 minutes (p less than 0.01). Mexiletine resulted in greater suppression of VPDs than lidocaine in terms of mean percent reduction (96% vs 68%, p less than 0.01). All lidocaine patients had therapeutic plasma levels (range 1.6 to 3.5 micrograms/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

The antiarrhythmic efficacy of oral acebutolol, a new cardioselective beta-blocking agent, was assessed in a randomized double-blind, placebo-controlled study. Twenty-five patients with greater than or equal to 30 ventricular ectopic beats (VEB) per hour on three control ambulatory monitorings were studied. Mean VEB reduction from the control period was 35% with placebo and 45% and 50% with the use of acebutolol 200 mg and 400 mg, respectively. Eleven patients had greater than or equal to 70% reduction in VEB with acebutolol and nine of them had greater than or equal to 90 VEB reduction. Among these 11 patients, the mean VEB suppression was 51% after placebo but significantly higher following the two doses of acebutolol at 71% (p less than 0.05) and 86% (p less than 0.01). The mean reduction of paired VEB compared to placebo was 71% (p less than 0.05) and 75% (p less than 0.01) following 200 mg and 400 mg of acebutolol and only 49% after placebo. Complete suppression of paroxysmal ventricular tachycardia was also noted in five patients. Mean PR interval only increased slightly when patients took 400 mg of acebutolol, but there was no significant change in either the QRS or QTc intervals. A significant decrease in heart rate from that during control periods was noted after acebutolol. No significant adverse reactions were noted during the study. Acebutolol appears to be an effective and well-tolerated antiarrhythmic agent in the treatment of VEB and higher grades of ventricular ectopy.

We examined the potential for laser irradiation of congenital heart defects, with the use of postmortem hearts and an argon ion laser with a flexible quartz fiber. Atrial septectomy was performed in five newborn hearts. Obstructive lesions were relieved by laser irradiation in valvular pulmonic and aortic stenosis, dysplastic pulmonary valve, pulmonary atresia, and coarctation of the aorta. To demonstrate the efficacy of in vivo cardiac laser surgery, atrial septectomy was also performed in an anesthetized dog model, under echocardiographic visualization, without change in heart rate or blood pressure. Our results demonstrate the feasibility of intracardiac and intravascular laser irradiation for palliation and repair of selected congenital heart diseases.

Since coronary thrombosis is a principal factor in the evolving necrotic process in the majority of patients with acute myocardial infarction (AMI), a prospective study was conducted in 25 AMI patients who underwent expeditious coronary arteriography. Of these patients, 22 with totally occluding thrombus also received early streptokinase (STK) administration. STK was given by intracoronary (20 patients) or systemic (two patients) infusion, 2000 to 50,000 IU/min, to a total dose of 125,000 to 500,000 IU within 10 hours of AMI symptom onset. Eighteen patients had angiographically visualized successful coronary thrombolysis; the shorter the interval between onset of symptoms to treatment, the more rapid was the clot dissolution. Successful thrombolysis occurred concomitantly with readily managed reperfusion ventricular tachyarrhythmias in nearly all patients. In addition, STK recanalization resulted in relief of ongoing chest pain in 10 of 12 patients, 10 of 16 evidenced immediate normalization of hyperacute ST segment abnormalities, and 8 of 14 demonstrated subsequent improvement of angiographically visualized left ventricular (LV) ejection fraction. In the percutaneous transluminal coronary recanalization (PTCR) procedure, the step of using a soft-tipped guide wire itself was transiently useful in only one of seven patients in whom this was attempted; reocclusion took place without added STK therapy. Nitroglycerin (NTG) alone produced only slight distal patency in but 1 of 19 patients with coronary occlusion given the nitrate. Importantly, in 14 control AMI patients receiving conventional treatment without STK, 10 showed angiographically complete occlusion of the coronary artery supplying the infarct region 1 month after infarction, thereby excluding spontaneous clot lysis mimicking STK-PTCR-induced reperfusion. These data support the concept that coronary occlusion by thrombosis is inherently involved with AMI and that rapid PTCR application of intracoronary STK provides potent thrombolysis, superior to that provided by NTG and guide wire passage in reestablishing coronary flow with attendant salvage of jeopardized myocardium and with subsequently improved LV function.

Severe atherosclerotic obstructed coronary artery disease (CAD) may preclude passage of a balloon catheter for transluminal coronary angioplasty (TCA). Since lasers have been shown to effectively vaporize CAD plaque, the initial application of laser to effect a lumen large enough to accommodate the angioplasty catheter for further dilatation was explored. Eleven postmortem human CAD segments which did not permit passage of a 1.33 mm shaft diameter angioplasty catheter were studied. Argon laser radiation (14 to 90 J) transmitted via 400 micron core diameter quartz fiber onto the stenotic channel of 0.58 mm created a vaporized lumen of 1.77 mm (mean increase of 1.31 +/- 0.25 mm, p less than 0.001). The laser procedure allowed the balloon angioplasty catheter to be pushed into the stenosis. TCA was then performed (7 atm, 45 seconds) and expanded the channel to 2.12 mm (additional mean increase of 0.38 +/- 0.07 mm, p less than 0.001). In terms of percent luminal narrowing, laser radiation reduced obstruction from 80% to 45% (mean difference of -38.7 +/- 4.6%, p less than 0.001), and TCA caused a further decrease to 37% (mean difference of -9.3 +/- 1.9%, p less than 0.001). Thus, in tight atherosclerotic lesions, the laser may be useful in creating an initial opening enabling the placement of the balloon angioplasty catheter which, in turn, can further dilate the lased stenotic coronary lumen.

The fiberoptic scope is increasingly used in the coronary and peripheral arteries to quantitate the degree and type of arterial obstructive disease and to inspect the results of procedures such as bypass grafting and laser irradiation of obstructive lesions. Since little is known about this instrument's potential complications, we passed a variety of fiberoptic scopes (1.8 to 3.6 mm outer diameter) in fresh postmortem pig coronary arteries and live monkey and canine peripheral arteries, and observed the intraluminal anatomy through the angioscope. No perforations were created, but ridges rising from the vascular luminal surface, avulsion of the endothelial lining, and small flaps attached at one end to the vessel wall were observed. Histologically, subintimal and medial tears were evident. Inserting large diameter scopes or making frequent passes (10 to 100) in coronary arteries increased intravascular injury. The use of small diameter flexible scopes or infrequent passes (less than 10) in the larger iliac and femoral arteries of live monkeys and dogs resulted in a lower frequency of myointimal sloughing or flap formation. Current fiberoptic scopes are not ideal angioscopes; they have a rigid tip, cannot be steered adequately, and are relatively stiff, resulting in a high probability of intraluminal injury, especially when used in small tortuous arteries. To decrease the risk of such injury, we recommend gentle manipulations while passing the scope and use of the smallest diameter scope possible. We further suggest limited use of the fiberscope, or at least limiting the number of passes in small vessels such as coronary arteries.

Fresh autologous thrombus, 1.0 to 1.5 ml, was injected into the left anterior descending and/or left diagonal coronary arteries of 19 open-chest dogs to produce evolving acute myocardial infarction (AMI). Thrombotic obstruction was documented by coronary angiography. Multilead epicardial ECGs showed ST segment elevations of affected left ventricular (LV) areas within 2 minutes after thrombus injection, and LV segmental wall cyanosis with hypocontraction was observed within 10 minutes in the myocardial areas supplied by the thrombosed artery. Ten animals then received an initial dose of streptokinase (STK), 250,000 U (intravenous), followed by STK, 1000 to 3000 U/min (intracoronary), while nine control dogs untreated with STK received normal saline infusion. All but one STK-treated animal (all nine animals receiving intracoronary STK) had reestablishment of blood flow in the previously occluded vessels within 1 1/2 hours, disappearance of ventricular cyanosis, return of normal LV contractile function, and normalization of elevated ST segments within 1 hour after intracoronary STK therapy. In contrast, in the non-STK-treated control group, all animals had continued coronary obstruction, progressive ST elevations, and worsening LV cyanosis and hypocontraction until death or for more than 3 hours post thrombus; three control animals died of ventricular fibrillation (VF) within 1 hour of thrombus occlusion, three more died of VF within 2 hours post thrombus, and only three survived beyond 2 hours post thrombus. Postmortem examination of non-STK-treated animals revealed extensive residual coronary thrombus. All intracoronary STK-treated animals evidenced absence of residual coronary thrombus at postmortem examination. These data provide clinically relevant evidence that early intracoronary STK effects thrombolysis in AMI by reopening coronary vessels occluded by fresh thrombus, thereby protecting myocardium from further ischemia and necrosis, preserving LV function, and also reversing cardiac muscle injury.

To determine the effects of laser irradiation upon human coronary atherosclerotic disease, coronary plaques were extracted from fresh human cadaver hearts. Seventy-four diseased artery samples were sectioned either transversely or longitudinally and subjected to laser treatment from argon-ion and carbon dioxide sources. The laser beam affected vaporization and patency in fibrous, lipoid, and calcified plaques as observed histologically. Calcified blockage showed greater extent of charred remnants following controlled thermal injury than did fibrous or lipoid obstructions. The area and depth of penetration varied directly with intensity and duration of photoirradiation and inversely with the density of the atherosclerotic tissue. This study supports further research work on the use of lasers to effect relief of atherosclerotic obstructions.