Leonard M. Shapiro

Cardiac Remote Ischemic Preconditioning in Coronary Stenting (CRISP Stent) Study: a prospective, randomized control trial.

Background— Myocyte necrosis as a result of elective percutaneous coronary intervention (PCI) occurs in approximately one third of cases and is associated with subsequent cardiovascular events. This study assessed the ability of remote ischemic preconditioning (IPC) to attenuate cardiac troponin I (cTnI) release after elective PCI. Methods and Results— Two hundred forty-two consecutive patients undergoing elective PCI with undetectable preprocedural cTnI were recruited. Subjects were randomized to receive remote IPC (induced by three 5-minute inflations of a blood pressure cuff to 200 mm Hg around the upper arm, followed by 5-minute intervals of reperfusion) or control (an uninflated cuff around the arm) before arrival in the catheter laboratory. The primary outcome was cTnI at 24 hours after PCI. Secondary outcomes included renal dysfunction and major adverse cardiac and cerebral event rate at 6 months. The median cTnI at 24 hours after PCI was lower in the remote IPC compared with the control group (0.06 versus 0.16 ng/mL; P=0.040). After remote IPC, cTnI was <0.04 ng/mL in 44 patients (42%) compared with 24 in the control group (24%; P=0.01). Subjects who received remote IPC experienced less chest discomfort (P=0.0006) and ECG ST-segment deviation (P=0.005) than control subjects. At 6 months, the major adverse cardiac and cerebral event rate was lower in the remote IPC group (4 versus 13 events; P=0.018). Conclusion— Remote IPC reduces ischemic chest discomfort during PCI, attenuates procedure-related cTnI release, and appears to reduce subsequent cardiovascular events.

Association Between IVUS Findings and Adverse Outcomes in Patients With Coronary Artery Disease The VIVA (VH-IVUS in Vulnerable Atherosclerosis) Study

OBJECTIVES The purpose of this study was to determine whether thin-capped fibroatheromata (TCFA) identified by virtual histology intravascular ultrasound (VH-IVUS) are associated with major adverse cardiac events (MACE) on individual plaque or whole patient analysis. BACKGROUND Post-mortem studies have identified TCFA as the substrate for most myocardial infarctions. However, little is known about the natural history of individual TCFA and their link with MACE. VH-IVUS provides a method of identifying plaques in vivo that are similar (although not identical) to histologically defined TCFA, and has been validated in human atherectomy and post-mortem studies. METHODS One hundred seventy patients with stable angina or troponin-positive acute coronary syndrome referred for percutaneous coronary intervention (PCI) were prospectively enrolled and underwent 3-vessel VH-IVUS pre-PCI and also post-PCI in the culprit vessel. MACE consisted of death, myocardial infarction, or unplanned revascularization. RESULTS In all, 30,372 mm of VH-IVUS were analyzed. Eighteen MACE occurred in 16 patients over a median follow-up of 625 days (interquartile range: 463 to 990 days); 1,096 plaques were classified, and 19 lesions resulted in MACE (13 nonculprit lesions and 6 culprit lesions). Nonculprit lesion factors associated with nonrestenotic MACE included VHTCFA (hazard ratio [HR]: 7.53, p = 0.038) and plaque burden >70% (HR: 8.13, p = 0.011). VHTCFA (HR: 8.16, p = 0.007), plaque burden >70% (HR: 7.48, p < 0.001), and minimum luminal area <4 mm(2) (HR: 2.91, p = 0.036) were associated with total MACE. On patient-based analysis, the only factor associated with nonrestenotic MACE was 3-vessel noncalcified VHTCFA (HR: 1.79, p = 0.004). CONCLUSIONS VH-IVUS TCFA was associated with nonrestenotic and total MACE on individual plaque analysis, and noncalcified VHTCFA was associated with nonrestenotic and total MACE on whole-patient analysis, demonstrating that VH-IVUS can identify plaques at increased risk of subsequent events. The preservation of the association between VHTCFA and MACE despite various analyses emphasizes its biological importance.

Results of Prevention of REStenosis with Tranilast and its Outcomes (PRESTO) Trial

Background—Restenosis after percutaneous coronary intervention (PCI) is a major problem affecting 15% to 30% of patients after stent placement. No oral agent has shown a beneficial effect on restenosis or on associated major adverse cardiovascular events. In limited trials, the oral agent tranilast has been shown to decrease the frequency of angiographic restenosis after PCI. Methods and Results—In this double-blind, randomized, placebo-controlled trial of tranilast (300 and 450 mg BID for 1 or 3 months), 11 484 patients were enrolled. Enrollment and drug were initiated within 4 hours after successful PCI of at least 1 vessel. The primary end point was the first occurrence of death, myocardial infarction, or ischemia-driven target vessel revascularization within 9 months and was 15.8% in the placebo group and 15.5% to 16.1% in the tranilast groups (P =0.77 to 0.81). Myocardial infarction was the only component of major adverse cardiovascular events to show some evidence of a reduction with tranilast (450 mg BID for 3 months): 1.1% versus 1.8% with placebo (P =0.061 for intent-to-treat population). The primary reason for not completing treatment was ≥1 hepatic laboratory test abnormality (11.4% versus 0.2% with placebo, P <0.01). In the angiographic substudy composed of 2018 patients, minimal lumen diameter (MLD) was measured by quantitative coronary angiography. At follow-up, MLD was 1.76±0.77 mm in the placebo group, which was not different from MLD in the tranilast groups (1.72 to 1.78±0.76 to 80 mm, P =0.49 to 0.89). In a subset of these patients (n=1107), intravascular ultrasound was performed at follow-up. Plaque volume was not different between the placebo and tranilast groups (39.3 versus 37.5 to 46.1 mm3, respectively;P =0.16 to 0.72). Conclusions—Tranilast does not improve the quantitative measures of restenosis (angiographic and intravascular ultrasound) or its clinical sequelae.

Cardiac tumours: diagnosis and management

Until the 1950s, cardiac tumours were merely a curiosity. Diagnosis was academic and outlook poor. With the advent of cardiopulmonary bypass, however, surgical management became possible, particularly of intracavity tumours. More recently, the development of echocardiography, compututed tomography, and magnetic resonance imaging has contributed greatly to the process of preoperative diagnosis. Primary cardiac tumours are rare, with a necropsy incidence of 0.05%.1 Secondary deposits are seen more frequently, in 1% of postmortem examinations, but usually in the setting of widely disseminated malignancy.2 The relative incidence of presentation is shown in table 1, and demonstrates that atrial myxoma is by far the most common primary cardiac tumour in adults, and rhabdomyosarcoma is the most common in children. A quarter of all cardiac tumours are malignant, the majority of which are angiosarcomas or rhabdomyosarcomas. View this table: Table 1 Approximate incidence of benign tumours of the heart in adults and children ### General clinical features Cardiac tumours are diverse in clinical presentation, and atrial myxomas in particular may cause systemic symptoms mimicking collagen vascular disease, malignancy or infective endocarditis. There are several clinical features, however, that are seen commonly with many cardiac tumours:

Early Complications After Dual Chamber Versus Single Chamber Pacemaker Implantation

This study was performed to compare the frequency of early complications after single chamber versus dual chamber permanent pacemaker implantation. Early complication was defined as one occurring in the 6‐week period following implantation. We prospectively analyzed consecutive pacemaker implantation from January 1987 to June 1993 at our regional center. All complications were also analyzed for the relationship to operator experience, the venous access route, and the presence of temporary pacing wire at the time of implantation of the permanent pacing system. A total of 2019 new pacemaker units were implanted during this period. 1733 patients (85.8%) received a VVI pacemaker and 286 (14.2%) a DDD unit. Wound infection occurredin 11 (0.6%) VVI patients and 6 (2.1%) DDD patients. Lead displacement occurred in 18(1 %) VVI patients and 15 (5.2%) DDD patients (11 [3.8%] atrial and 4 [1.4 %] ventricular). There were 10 (0.6%)pneumothoraces, 9 (0.5%) hematomas requiring drainage, 1 (0.06%) chylocele, and 2 (0.1%) deaths in the VVI group. There were 2 (0.7%) pneumothoraces, 2 (0.7%) hematomas, and no deaths in the DDD group. There was no significant increase in complications for experienced infrequent implanters (< 12 systems per year). In both groups the subclavian approach was associated with a risk of pneumothorax when compared to the cephalic approach. The rate of wound infection was higher in patients who had a temporary pacing wire in place. The use of prophylactic antibiotics does not appear to affect the incidence of wound infection. The early complications in the DDD group were higher than in the VVI group (8.7% vs 2.9%, P < 0.05), being mainly due to an increased incidence of wound infection and atrial lead displacement.

Late complications following permanent pacemaker implantation or elective unit replacement

Objective To determine the rate of late complications following first implantation or elective unit replacement of a permanent pacemaker system. Design Analysis of pacemaker data and complications prospectively acquired on a computerised database. Complications were studied over an 11 year period from January 1984 to December 1994. Setting Tertiary referral cardiothoracic centre. Patients Records of 2621 patients were analysed retrospectively. Main outcome measures Complications requiring repeat procedures occurring more than six weeks after pacemaker implantation or elective unit replacement. Results The overall rate of late complications was significantly lower after first implantation of a permanent pacemaker (34 cases, complication rate 1.4%, 95% confidence interval 0.9% to 1.9%) than after elective unit replacement (16 cases, complication rate 6.5% (3.3% to 9.7%). There were 20 cases of erosion, 18 infections, five electrode problems, and seven miscellaneous problems. Complications were more common with inexperienced operators (18.9% (6.0% to 31.8%)) than with experienced operators (0.9% (0.3% to 1.5%)). Conclusions The incidence of late complications following pacemaker implantation is low and compares favourably with early complication rates. The majority are caused by erosion and infection. Patients who have undergone elective unit replacement are at particular risk.

Coronary flow reserve improves after aortic valve replacement for aortic stenosis: an adenosine transthoracic echocardiography study

OBJECTIVES The goal of this study was to assess coronary flow reserve (CFR) before and after aortic valve replacement (AVR). BACKGROUND Coronary flow reserve is impaired under conditions of left ventricular (LV) hypertrophy. It is not known whether CFR improves with regression of LV hypertrophy in humans. METHODS We investigated 35 patients with pure aortic stenosis, LV hypertrophy and normal coronary arteriograms. Patients underwent adenosine transthoracic echocardiography on two occasions--immediately before AVR and six months postoperatively. Left ventricular mass, distal left anterior descending coronary artery (LAD) diameter, flow and CFR were assessed on each occasion. RESULTS Distal LAD diameter was successfully imaged in 30 patients (86%), and blood flow was successfully imaged in 27 (77%). Paired data were subsequently available in 24 patients, of whom 14 were men, mean age 68.1+/-12.5 years, body mass index 24.5+/-2.0 kg/m2, aortic valve gradient 93+/-32 mm Hg. Pre- to post-AVR a significant decrease was seen in LV mass (271+/-38 vs. 236+/-32g, p<0.01) and LV mass index (154+/-21 vs. 134+/-21 g/m2, p< 0.01). Distal LAD diameter fell from 2.27+/-0.37 to 2.23+/-0.35 mm, p = 0.08). Pre- to post-AVR there was no significant change in resting parameters of peak diastolic velocity (0.43+/-0.16 vs. 0.41+/-0.11 m/s), distal LAD flow 23.3+/-10.1 vs. 20.9+/-5.2 ml/min or distal LAD flow scaled for LV mass (8.7+/-3.8 vs. 9.0+/-2.5 ml/min/100 g LV mass), but there was significant increase in hyperemic peak diastolic velocity (0.71+/-0.26 vs. 1.08+/-0.24 m/s; p<0.01), distal LAD flow (37.8+/-11.3 vs. 53.5+/-16.1 ml/min; p<0.01) and distal LAD flow scaled for LV mass (14.3+/-5.0 vs. 23.3+/-8.5 ml/min/100 g LV mass; p<0.01). Coronary flow reserve, therefore, increased from 1.76+/-0.5 to 2.61+/-0.7. CONCLUSIONS Coronary flow reserve increases after AVR for aortic stenosis. This increase occurs in tandem with regression of LV hypertrophy.

Physiological left ventricular hypertrophy.

Echocardiograms were recorded in 154 active athletes (from various sports) and 21 ex-athletes and compared with those in 40 normal control subjects (non-athletes). Diastolic cavity dimension and posterior wall and septal thickness were measured and left ventricular mass and the ratio of posterior wall thickness to cavity radius and of septum to posterior wall thickness calculated. As a group athletes had a significantly increased diastolic cavity dimension, posterior wall and septal thickness, and left ventricular mass. The ratio of posterior wall thickness to cavity radius was distributed as a single continuous variable with a significantly increased mean, and there was no separate subgroup of shot putters or weight lifters with inappropriate hypertrophy. The mean ratio of septum to posterior wall thickness was normal, but there was a wide range of values up to 2.1:1. Ex-athletes had entirely normal left ventricular dimensions and wall thickness. When athletes are categorised by their standard of competition national standard competitors had a significantly increased posterior wall and septal thickness and left ventricular mass compared with university and non-competitive sportsmen. In conclusion, strenuous activity results in left ventricular hypertrophy which is appropriate to the body size of the athlete and the degree of activity but not to its type.

Coronary angiography from the radial artery – experience, complications and limitations

AIMS to assess the outcomes, complications and limitations of coronary angiography performed via percutaneous radial artery puncture. METHODS AND RESULTS two hundred and fifty patients underwent diagnostic coronary angiography from the radial artery, 182 (72.8%) of whom had contraindications to the femoral approach, for example due to peripheral vascular disease (n=85), therapeutic anticoagulation (29), or failed femoral approach (17). Procedural success in this high-risk population was achieved in 231 patients (92.4%). Principle reasons for failure were unsuccessful radial access (5) and arterial spasm (5). Procedure duration (SD) for an operators first 20 cases compared with cases thereafter (min) was 47.7 (16.7) vs. 41.5 (14.6), P=0.0004; fluoroscopy time (min) 9.7 (7.1) vs. 6.6 (5.1), P=0.0001 and procedural success 89.6% vs. 94.1%, P=ns. Complications included two deaths associated temporally with catheterisation, three cases of arterial dissection without ischaemic sequelae and one transient ischaemic attack. CONCLUSIONS coronary angiography can be performed successfully from the radial artery, but this approach has limitations, which include the need to demonstrate dual palmar vascular supply, the prolonged learning phase, the procedural failure rate, patient discomfort and a demonstrable incidence of vascular and haemodynamic complications. We believe that radial coronary angiography should only be undertaken when there is a contraindication to the femoral approach.

Silent myocardial ischaemia in chronic stable angina: a study of its frequency and characteristics in 150 patients.

One hundred and fifty unselected patients with documented coronary artery disease were studied to establish the frequency and characteristics of silent myocardial ischaemia. Patients underwent ambulatory ST segment monitoring off all routine antianginal treatment (total 6264 hours) and exercise testing (n = 146). Ninety one patients (61%) had a total of 598 episodes of significant ST segment change, of which 446 (75%) were asymptomatic. Twenty seven patients (18%) had only painless episodes; 14 (9%) patients only painful episodes; 50 patients (33%) had both painless and painful episodes. The mean number of ST segment changes per day was 2.58 (1.95 silent); however, 11 patients (7%) had 50% of all silent episodes, and 48 patients (32%) had 91% of all silent episodes. Fifty nine patients (39%) had no ST segment changes on ambulatory monitoring, and 73 patients (49%) had no evidence of silent ischaemia. Episodes of silent ischaemia occurred with a similar circadian distribution to that of painful ischaemia, predominantly between 0730 and 1930. There was a similar mean rise in heart rate at the onset of both silent and painful episodes of ischaemia. Silent ischaemia was significantly more frequent in patients with three vessel disease than in those with single vessel disease, and was also significantly related to both time to 1 mm ST depression and maximal exercise duration on exercise testing. There was a highly significant relation between the mean number and duration of episodes of silent ischaemia in patients with positive exercise tests when compared with those with negative tests. No episode of ventricular tachycardia was recorded in association with silent ischaemic change.