Thomas L. McKiernan

The multicenter study of enhanced external counterpulsation (MUST-EECP): effect of EECP on exercise-induced myocardial ischemia and anginal episodes ☆

OBJECTIVES The purpose of this study was to assess safety and efficacy of enhanced external counterpulsation (EECP). BACKGROUND Case series have shown that EECP can improve exercise tolerance, symptoms and myocardial perfusion in stable angina pectoris. METHODS A multicenter, prospective, randomized, blinded, controlled trial was conducted in seven university hospitals in 139 outpatients with angina, documented coronary artery disease (CAD) and positive exercise treadmill test. Patients were given 35 h of active counterpulsation (active CP) or inactive counterpulsation (inactive CP) over a four- to seven-week period. Outcome measures were exercise duration and time to > or =1-mm ST-segment depression, average daily anginal attack count and nitroglycerin usage. RESULTS Exercise duration increased in both groups, but the between-group difference was not significant (p > 0.3). Time to > or =1-mm ST-segment depression increased significantly from baseline in active CP compared with inactive CP (p = 0.01). More active-CP patients saw a decrease and fewer experienced an increase in angina episodes as compared with inactive-CP patients (p < 0.05). Nitroglycerin usage decreased in active CP but did not change in the inactive-CP group. The between-group difference was not significant (p > 0.7). CONCLUSIONS Enhanced external counterpulsation reduces angina and extends time to exercise-induced ischemia in patients with symptomatic CAD. Treatment was relatively well tolerated and free of limiting side effects in most patients.

Acute procedural results in the treatment of 30 coronary artery bifurcation lesions with a double-wire atherectomy technique for side-branch protection

Percutaneous treatment of bifurcation lesions has been consistently shown to be associated with lower acute success rates, higher initial complication rates, and an increased rate of restenosis when compared with findings in nonbifurcation lesions. Recent analysis of data from a CAVEAT subgroup suggests that directional atherectomy of bifurcation lesions can improve initial success rates and lower restenosis rates but at the cost of high complication rates. Reports from several angioplasty series document improved success rates and lower complication rates with the use of a two-wire technique to protect side branches when treating bifurcation lesions. Our experience with a two-wire atherectomy technique that uses a nitinol wire to protect important side branches is presented.

Apical hypertrophic cardiomyopathy in American patients

Ce type de cardiomyopathie dont sont atteints 3% des Japonais existe aussi chez les Americains: observation chez 2 blancs et 1 noir

Infiltrator angioplasty balloon catheter : A device for combined angioplasty and intramural site-specific treatment

OBJECTIVES We describe a new angioplasty device (Infiltrator Angioplasty Balloon Catheter; IABC) with intramural drug delivery capability. The conventional balloon part of the device, when inflated, dilates the vessel or has three rows of longitudinally mounted infiltrator nipples to penetrate the tunica media. Through an independent infiltrator port and nipples, drugs can be infiltrated directly into the vessel wall. METHODS The device was tested in 117 normal coronary arteries of 58 farm pigs. RESULTS (1) The infiltration procedure does not damage the vessel angiographically or histologically. At the infiltration site, the endothelial layer and the internal elastic lamina has a controlled interruption, and the infiltrated fluid is distributed among the medial layers, causing a mild focal edema and medial thickening (1.8 times on average). (2) Rhodamine tracer is circularly and evenly distributed through the whole width of the vessel wall within 10 min after infiltration. (3) Two weeks after the infiltration procedure, the medial layer reveals mild local thickening and remodelling without luminal narrowing. (4) Of the intramurally infiltrated Tcm99-labeled surfurcolloid, 83.8% is detectable at 5 min after the delivery procedure by gamma camera. (5) The IABC, if oversized, is able to achieve angiographic dilatation in normal pig coronary arteries, causing histologic damage similar to or less than that induced by conventional balloon dilatation. CONCLUSIONS The IABC can deliver fluid-phase substances directly into the vessel wall with microliter accuracy and with 90% efficiency without significant acute and subacute damage to the vessel wall. It is also suitable for combined dilatation and local drug delivery.

Asymmetry of Right Ventricular Enlargement in Response to Tricuspid Regurgitation

BACKGROUND Analysis of right ventricular adaptation to tricuspid regurgitation was studied in 10 heart transplant recipients following inadvertent endomyocardial biopsy disruption of the tricuspid apparatus. METHODS AND RESULTS Echocardiography demonstrated progressive diastolic right ventricular cavity enlargement (19.5+/-5.0 to 30.3+/-5.4 cm(2), P<0.0002), with disproportionate elongation along the midminor axis (3.5+/-0.6 to 5. 0+/-0.5 cm, P<0.001). As the right ventricle remodeled to more spherical (and less elliptical) proportions, the end-diastolic right ventricular midminor axis/long axis ratio increased significantly from 0.52+/-0.10 to 0.68+/-0.07, P<0.005. CONCLUSIONS Ventricular enlargement due to right ventricular volume overload results in disproportionate dilation along the free wall to septum minor axis.

Report of successful use of argatroban as an alternative anticoagulant during coronary stent implantation in a patient with heparin‐induced thrombocytopenia and thrombosis syndrome

Heparin-induced thrombocytopenia and thrombosis syndrome (HITTS) is a severe complication of heparin caused by an antibody response to the heparin-platelet factor 4 complex which results in severe thrombosis. Heparin rechallenge in HITTS patients carries a high risk of inducing thrombosis. Antithrombin agents represent treatment alternatives in HITTS patients who require anticoagulation. We report successful coronary stent implantation in a HITTS patient using the antithrombin agent argatroban.

Serpentine Thrombus Traversing the Foramen Ovale: Paradoxical Embolism Shown by Transesophageal Echocardiography

Paradoxical embolism is a rare cause of myocardial infarction. We describe a patient in whom morbid obesity obscured clinical examination and rendered invasive diagnostic evaluation by angiography unfeasible. Transesophageal echocardiography showed the pathophysiologic basis for respiratory decompensation (pulmonary thromboembolism) and myocardial infarction (paradoxical embolism to a coronary artery) after transthoracic echocardiography and computed axial tomography had failed to distinguish among the initial differential diagnostic possibilities. These possibilities included left ventricular systolic dysfunction, pulmonary embolism, pulmonary sepsis, and acute decompensation of chronic pulmonary disease caused by morbid obesity. Case Report A 48-year-old man presented with progressive dyspnea and no history of other difficulties. Three weeks before admission, he had lost consciousness briefly and had had associated numbness in both hands and chest pain radiating to the left shoulder. The chest pain had resolved rapidly but had recurred intermittently over the following 3 days. The patient weighed 177 kg; his body temperature was 38.5 C, his respiratory rate was 30 breaths/min, his heart rate was 116 beats/min, and his blood pressure was 160/100 mm Hg. Breath sounds were diffusely diminished, and rales were heard bilaterally throughout the lower third of the thorax. Cardiac rhythm was rapid and regular and was associated with biventricular third heart sounds. Pitting edema was seen on the abdominal wall. The patients extremities were cyanotic peripherally, but clubbing was absent. Moderate to severe pitting edema was present from the feet to the thighs. Arterial blood gas samples taken while the patient was breathing room air showed a pH of 7.28 (normal range, 7.35 to 7.45), a Pco 2 of 64 mm Hg (normal range, 30 to 50 mm Hg), and a Po 2 of 51 mm Hg (normal range, 80 to 100 mm Hg). A chest radiograph showed cardiomegaly and bilateral pleural effusions. An electrocardiogram showed sinus tachycardia, right axis deviation, bi-atrial enlargement, and nonspecific ST-T wave changes. The patient required intubation and mechanical ventilation after his respiratory condition deteriorated, but hypoxemia persisted despite the administration of an inspired fractional oxygen concentration of 100%. The patients central venous pressure was 19 mm Hg (normal range, 2 to 8 mm Hg); his peak right atrial pressure was 25 mm Hg (normal range, less than 10 mm Hg); his right ventricular pressure was 68/12 mm Hg (normal range, 15/2 to 30/8 mm Hg); and his pulmonary artery pressure was 60/36 mm Hg (normal range, 15/4 to 30/12 mm Hg). Transesophageal echocardiography showed a nondilated left ventricle compressed by a markedly enlarged right ventricle. A multilobed mobile mass adjacent to the catheter in the right atrium prolapsed across a tricuspid valve that otherwise appeared normal (Figure 1). The same mass formed a serpentine structure that traversed a patent foramen ovale, entered the left atrium, and crossed the mitral valve. Shaggy echo densities were imaged near the anterior mitral valve leaflet and the aortic valve. These echo densities were shown to be continuous, with the mass originating in the right atrium. Intravenous administration of systemic venous saline contrast fully opacified the right atrium and spontaneously crossed through the patent foramen ovale to the left atrium during positive-pressure ventilation. At this time, the patients pulmonary arterial pressure was 70/46 mm Hg, and his systemic arterial pressure was 85/46 mm Hg. Figure 1. Transesophageal echocardiogram of paradoxical embolism. left panels right panels P A L R Top. Middle. Bottom. arrow The patient was not considered to be a candidate for surgery and died despite aggressive medical management. Autopsy showed a markedly enlarged heart with severe right ventricular dilation and hypertrophy causing substantial compression of the left ventricular cavity. A large thrombus, weighing 36 g, partially obstructed the tricuspid orifice and extended into the right atrium, the chordae tendineae, and the papillary musculature of the tricuspid valve (Figure 2). Patency of the foramen ovale was seen when a probe was used to displace the septum primum 1.2 cm from the limbus of the septum secundum. Examination of the lungs in situ showed multifocal hemorrhagic areas consistent with acute pulmonary infarctions. The lumen of a diagonal branch of the left anterior descending coronary artery contained a recent embolic thrombus, and there was evidence that an organizing myocardial infarction had occurred approximately 2 to 3 weeks earlier. The presumed mechanism of death was respiratory failure due to acute pulmonary thromboembolism complicated by acute myocardial infarction. Figure 2. The heart after the patients death, showing intracardiac thrombus and patent foramen ovale. Top. Bottom. Discussion The direct demonstration of paradoxical embolism by imaging a thrombus traversing the foramen ovale is unusual [1-3]. In our patient, transesophageal echocardiography showed three criteria for the diagnosis of paradoxical embolism [4, 5]. First, a large intracardiac thrombus (the embolic source) was seen in both the right and left sides of the heart. Second, the potential communication, a patent foramen ovale, was shown by the spontaneous transit of saline contrast between the atria, the physical presence of thrombus extending across the atrial septum at the fossa ovalis, and systemic hypoxemia despite a fractional inspired oxygen concentration of 100% [6-9]. Third, right ventricular enlargement and leftward ventricular septal displacement indicating severe pulmonary hypertension was the driving force for interatrial shunting and paradoxical embolism [10]. Evidence of several pulmonary infarctions found at autopsy provided one explanation for the pulmonary hypertension. Systemic embolism to the coronary vasculature and subsequent myocardial infarction shown by histologic studies resulted from embolization of the thrombus in the left side of the heart that was imaged by transesophageal echocardiography. This patient was unusual because of the marked size and extent of the thrombus seen by transesophageal echocardiography in the right atrium and right ventricle and because of the demonstration of the propagation of the thrombus across a patent foramen ovale. Although the patients dire clinical circumstances precluded surgical intervention, the transesophageal echocardiogram was critical in showing the potential for catastrophic systemic embolism as the thrombus propagated across the interatrial septum. Dr. Izban: Loyola University Medical Center, Department of Pathology, 2160 South First Avenue, Maywood, IL 60153. Dr. Reyes: 578-113 Room D121, Hines Veterans Administration Hospital, Hines, IL 60141. Dr. McKiernan: Loyola University Medical Center, Division of Cardiology, Building 110, Room 6232, 2160 South First Avenue, Maywood, IL 60153. Dr. Louie: Loyola University Medical Center, Division of Cardiology, Building 110, Room 6228, 2160 South First Avenue, Maywood, IL 60153.