To visualize intracoronary lesions in patients with different clinical expressions of coronary disease, we performed coronary angioscopy during coronary-artery bypass surgery in 10 patients with unstable angina and 10 patients with stable coronary disease. We examined a total of 32 vessels, using flexible fiberoptic angioscopes. Twenty-two vessels had no acute intimal lesion; three had complex plaques, six had thrombi, and one had both. Coronary angiography correctly identified the absence of complex plaque and thrombus in 22 vessels, but it detected only one of four complex plaques and one of seven thrombi. On angioscopy, none of the 17 arteries in the patients with stable coronary disease had either a complex plaque or thrombus. In the "offending" arteries of the patients with unstable angina, all three patients with accelerated angina had complex plaques and all seven with angina at rest had thrombi. We conclude that angioscopy frequently reveals complex plaques or thrombi not detected by coronary angiography. Our observations suggest that anginal syndromes that are refractory to medical treatment can be caused by unstable pathologic processes in the intima. Ulceration of plaques may increase the frequency and severity of effort angina, and the subsequent development of partially occlusive thrombi may cause unstable rest angina.

Although revascularization of hypoperfused but metabolically active human myocardium improves segmental function, the temporal relations among restoration of blood flow, normalization of tissue metabolism and recovery of segmental function have not been determined. To examine the effects of coronary angioplasty on 13 asynergic vascular territories in 12 patients, positron emission tomography and two-dimensional echocardiography were performed before and within 72 h of revascularization. Ten patients underwent late echocardiography (67 +/- 19 days) and eight underwent a late positron emission tomographic study (68 +/- 19 days). The extent and severity of abnormalities of wall motion, perfusion and glucose metabolism were expressed as wall motion scores, perfusion defect scores and perfusion-metabolism mismatch scores. Angioplasty significantly increased mean stenosis cross-sectional area (from 0.95 +/- 0.9 to 2.7 +/- 1.4 mm2) and mean cross-sectional luminal diameter (from 0.9 +/- 0.6 to 1.9 +/- 0.5 mm) (both p less than 0.001). Perfusion defect scores in dependent vascular territories improved early after angioplasty (from 116 +/- 166 to 31 +/- 51, p less than 0.002) with no further improvement on the late follow-up study. The mean perfusion-metabolism mismatch score decreased from 159 +/- 175 to 65 +/- 117 early after angioplasty (p less than 0.01) and to 26 +/- 29 at late follow-up (p less than 0.001 vs. before angioplasty; p = NS vs. early after angioplasty). However, absolute rates of glucose utilization remained elevated early after revascularization, normalizing only at late follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

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Pheochromocytoma and functional paraganglioma are uncommon causes of secondary hypertension. In rare instances, these catecholamine-secreting tumors present as atypical and dramatic symptoms without clear history of hypertension. We describe here LV thrombus and embolic stroke caused by a functional paraganglioma. CASE HISTORYA 49-year-old Caucasian man was admitted for elective transesophageal echocardiography to examine whether he had a patent foramen ovale. One month before this admission, the patient had flulike symptoms, left upper quadrant abdominal pain, and constipation for 2 weeks. He then developed a 1-minute episode of garbled speech and left upper extremity weakness that lasted for 24 hours. He was admitted into another hospital. An abdominal computed tomography (CT) scan revealed a large left retroperitoneal mass and multiple left renal infarcts. A head CT suggested stroke. Since the renal and brain infarcts suggested an embolic etiology, transthoracic echocardiography was performed, which detected a 1.3Â1.9 cm mobile mass in the mid left ventricle apparently attached to the interventricular septum (Figure 1, Left). Also noted was reduction of left apical wall motion. Transesophageal echocardiography was performed at the other hospital without complications and confirmed the transthoracic findings. On electrocardiography (ECG), the patient exhibited a prolonged QT interval and diffuse T-wave abnormalities especially on the precordial leads without evidence of atrial fibrillation (Figure 1, Right). Troponin levels were mildly elevated to 0.07 ng ⁄ mL (normal <0.05 ng ⁄ mL). Coronary angiography revealed normal coronary arteries. He was anticoagulated with heparin, then warfarin and enoxaparin, and was treated with metoprolol due to the abnormal ECG findings. On repeat echocardiography and cardiac magnetic resonance imaging (MRI) 2 to 3 weeks later, the left ventricular (LV) mass was not seen, but LV systolic function was still abnormal, with an ejection fraction of 47%. The distal left ventricle and apex thickened during diastole but moved dyskinetically during early systole.

The purpose of this study was to define specific types of resetting responses to programmed electrical stimulation during human ventricular tachycardia and to use computer simulations of reentry circuits to assess the possible mechanisms and pacing site location relative to the reentry circuit for each type of response. The effects of scanning single stimuli at 35 left ventricular endocardial sites during sustained monomorphic ventricular tachycardia in 12 patients were studied. In considering alterations in QRS configuration and the delay between the stimulus and the advanced QRS, we identified three types of resetting responses to scanning stimuli consistent with stimulation at sites in or near the reentry circuit at 12 abnormal endocardial sites in eight patients. Type 1: all capturing stimuli were followed after a delay by early QRS complexes that had the same configuration as the tachycardia complexes. Type 2: late stimuli reset tachycardia as in type 1 but early stimuli reset the tachycardia after altering the QRS configuration. Type 3: late stimuli reset tachycardia as in type 1, but early stimuli advanced tachycardia with a short stimulus to QRS delay without altering the QRS configuration. In the simulations, premature depolarization of sites in the circuit produced orthodromic and antidromic wavefronts. The orthodromic wavefront propagated through the circuit and exited the circuit at the same site as did the previous tachycardia wavefronts and advanced the tachycardia without altering the configuration of the advanced QRS. The antidromic wavefront of relatively late stimuli was confined within or near the circuit by collision with the orthodromic wavefront of the preceding tachycardia beat and failed to alter ventricular activation distant from the circuit. Therefore, the QRS configuration after the stimulus was unchanged. A type 1 response occurred when all capturing stimuli produced this effect. However, with increasing stimulus prematurity, the antidromic wavefront propagated farther before colliding with an orthodromic wavefront, and under some conditions, it exited the circuit from a site other than the original circuit "exit," and altered the ventricular activation sequence distant from the circuit and, therefore, the QRS configuration, producing a type 2 pattern. The type 3 pattern occurred when the antidromic wavefront of early premature beats captured the original circuit exit. The effect of a stimulus was dependent on the stimulus prematurity, the relative conduction times from the stimulation site to the potential sites of "exit" from the circuit, and the timing of the excitable gap at the stimulation site. In the figure-eight reentry circuit simulations, the type 1 response tended to occur during stimulation within, the type 2 response near the entrance to, and the type 3 response outside but near the exit from the slowly conducting central common pathway. Type 2 responses could also occur with stimulation at a site that was close to but not within the circuit. The recognition of specific ...

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The standard exercise recommendation -20 to 30 minutes at 60% to 85% of maximum heart rate four or five times a week- should be part of asthma management. Not only will patients benefit in a general way, but improved fitness is likely to reduce airway reactivity and medication use. The capacity to exercise, however, requires good general control of asthma, including use of inhaled corticosteroids and avoidance of triggers. In addition, patients must be taught to prevent exercise-induced bronchoconstriction by using inhaled medications and strategies like avoiding cold-weather exercise.

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