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This article familiarizes the reader with several different cardiac devices including pacemakers and implantable cardioverter defibrillators, intra-aortic balloon pumps, ventricular assist devices, valve replacements and repairs, shunt-occluding devices and passive constraint devices. Many cardiac devices are routinely encountered in clinical practice. Other devices are in the early stages of development, but circumstances suggest that they too will become commonly found. The radiologist must be familiar with these devices and their complications.

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We describe a case of cocaine-associated acute myocardial infarction managed by cardiac catheterization and intracoronary thrombolysis. Based on this and other reported cases, it appears that an invasive approach to the management of cocaine-associated acute myocardial infarction is advantageous over intravenous thrombolysis. Such a strategy would define the pathophysiology of acute myocardial infarction in the setting of cocaine use and allow mechanical intervention should pharmacologic therapy be unsuccessful.

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A newborn infant presented with a life-threatening cardiac arrhythmia. Echocardiography showed a large cardiac mass growing exophytically in the region of the left atrial appendage extending along the left ventricular wall but showed no clear tissue plane between the mass and the left ventricular wall. Based on the echocardiogram, surgical resection might damage the left ventricular wall. Magnetic resonance imaging demonstrated a clear plane of demarcation, making surgical resection a viable life-saving option.

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We report a case of spontaneous coronary dissection occurring in a middle aged male which was treated with thrombolytic therapy and directional coronary atherectomy. This technique provides a new option for treating this entity in the cardiac catheterization laboratory.

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We report 2 cases of successful angioplasty of anomalous right coronary arteries originating above the sinotubular line at the junction of the right and left sinus of Valsalva. The use of Amplatz left guiding catheters provided optimal support for performing angioplasty.

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An unusual case of a mitral annular abscess caused by Streptococcus pneumoniae was diagnosed by transesophageal echocardiography. The patient underwent surgical resection of the abscess and developed outflow tract obstruction. This is an unusual complication of the surgical procedure. The outflow tract obstruction may have been due to anterior displacement of the mitral valve by the abscess.

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Two-dimensional echocardiography has become the standard technique for evaluation of cardiac and paracardiac mass lesions. We have used magnetic resonance imaging (MRI) as an independent assessment of cardiac-associated masses in patients with echocardiograms demonstrating sessile atrial tumors. MRI was performed in seven patients, ages 33 to 84, whose echocardiographic diagnoses included left atrial mass (five), right atrial mass (one), and interatrial mass (one). In four of the patients with a diagnosis of left atrial mass, MRI showed extracardiac compression of the atrium, simulating a tumor (hiatal hernia, tortuous descending aorta, bronchogenic cyst). MRI was entirely normal in one patient with an apparent left atrial mass. MRI elucidated extension of an extracavitary mass into the interatrial septum in two patients. One of these patients with an echocardiographic right atrial mass had extension of a lipoma into the interatrial septum without atrial tumor. MRI confirmed the echocardiographic diagnosis of an interatrial mass in the other patient. We conclude that MRI, because of its ability to define anatomic relationships and tissue characteristics, is a powerful noninvasive tool for evaluating suspected cardiac mass lesions. Although echocardiography remains the primary screening test for the detection of cardiac masses, MRI is a more specific modality for precise diagnosis. Correct MRI interpretation may obviate the need for invasive studies or surgery.

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An understanding of the anomalies of the coronary arteries is imperative for physicians dealing with diagnosis and treatment of coronary artery disease. Although not as common as acquired coronary artery disease, congenital coronary anomalies contribute to significant morbidity and mortality. In addition, they may present difficulties for the angiographer at the time of catheterization, as well as a challenge for the radiologist in interpretation. To facilitate a better understanding of these anomalies, a new classification is presented, together with illustrations and discussion of the clinical significance.

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Mitral valve prolapse (MVP) is a common valvular abnormality which is observed in as many as 5% of the general population. Although invasive as well as noninvasive tools have been developed to determine the existence of this disorder, none is perfect and false negative as well as false positive diagnoses abound. Because MVP is a relatively benign disorder, it has also not been easy to make the usual clinical-pathological correlations. Left ventriculography is considered by many to be the gold standard, but this designation is probably not deserved. The angiographic criteria used by most do not permit unequivocal separation of normal mitral valve systolic bulging from pathologic MVP, and the interobserver and intraobserver variability of interpretation is high. However, false positive diagnoses can be eliminated if MVP is diagnosed only when para-annular displacement of mitral leaflet tissue is detected during systole rather than simple leaflet bulging. Although mid-systolic clicks and late systolic murmurs have proven to be the auscultatory hallmarks of this disorder, many patients have these signs without other diagnostic findings, consequently making it impossible to confirm the presence of MVP. Furthermore, the appearance of diagnostic echocardiographic abnormalities in patients with normal cardiac examinations implies that auscultation is not a sensitive marker of MVP. Both M-mode and two-dimensional echocardiography have technical limitations and the repeatability of interpretation of these tests is disappointingly low (80 to 90%). Because of these difficulties the angiographic-echocardiographic correlation is only fair. Nonetheless echocardiography has generally been accepted as the diagnostic modality of choice. Future technical improvements will likely enhance the diagnostic accuracy of this technique.

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To correlate angiographic and hemodynamic events in hypertrophic cardiomyopathy (HC), 14 patients with HC were investigated using pressure recordings and caudocranial left anterior oblique contrast angiography. Patients were separated into 2 groups on the basis of the presence (group I) or absence (group II) of systolic anterior motion of the anterior mitral leaflet on caudocranial angiography. In group I (10 patients), the pressure gradient could be recorded with the left ventricular (LV) catheter in the nonobliterated inflow region of the left ventricle. Simultaneous micromanometer tracings and caudocranial angiography revealed that contact between the anterior mitral leaflet and the ventricular septum was an early systolic event (occurring 136 +/- 33 ms after the R wave of the electrocardiogram) and was coincident with the onset of the pressure gradient. Cavitary obliteration was present in only 7 of 10 patients in group I, and occurred late in systole well after the peak gradient (292 +/- 28 ms after the R wave). In group II (4 patients), the pressure gradients could be recorded only from the obliterated portion of the ventricle distal to the level of the papillary muscles. Total LV cavitary obliteration was present in all group II patients. In 1 patient, simultaneous micromanometer pressure recording and caudocranial angiography revealed that cavitary obliteration preceded the peak gradient by 40 ms. Thus, in group I patients the onset of the pressure gradient is coincident with mitral leaflet-septal contact, while cavitary obliteration is an inconsistent late systolic event.(ABSTRACT TRUNCATED AT 250 WORDS)

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Twenty-three cases of an anatomic variant of the left anterior descending artery (LAD) are described. This variant is termed "dual LAD" and consists of two branches which supply the usual distribution of the LAD. One branch (short LAD) terminates in the proximal aspect of the anterior interventricular sulcus (AIVS). A second, longer branch has a variable course outside the AIVS and returns to the AIVS distally. The long LAD arose from the LAD proper in 21 cases and from the RCA in two cases. The initial course of the long LAD was on the epicardial surface of the left ventricle (17 cases), right ventricle (three cases), or within the interventricular septum (three cases). Recognition of these variants is important for correct surgical identification of the short and long LADs.

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Differentiation of bicuspid aortic valve from other causes of calcific aortic stenosis is not possible by echocardiography or, in many cases, by aortography. This report describes newly recognized patterns of calcification on plain films that are diagnostic for a bicuspid aortic valve. These are based on identification of the calcified raphe and/or the calcified conjoint leaflet. In 120 patients who underwent surgical repair of calcific aortic stenosis, 40 were found to have bicuspid valve. Examination of the plain films retrospectively allowed a correct recognition of 26 (65%) of these valves. In contrast, only 10 (25%) could be recognized by aortography. Patterns of calcification on plain films represent an important tool for detection of calcified cogenital bicuspid aortic valve.

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To determine whether left ventricular cavitary obliteration (a finding previously described only in hypertrophic states) can be induced in normal subjects, 16 patients without coronary artery disease or clinical evidence of hypertrophic obstructive cardiomyopathy were studied during cardiac catheterization. Resting left ventricular and aortic pressures and left ventriculography were repeated during the strain phase of Valsalva maneuver after administration of amyl nitrite. Cavitary obliteration during normal sinus rhythm was defined as disappearance of the sinus portion of the left ventricle during systole, and graded as absent, partial or total. Patients were placed into two groups on the basis of qualitative analysis of the resting left ventriculogram: the 10 patients in group A had normal left ventriculograms and the six patients in group B had hyperkinetic left ventricles. During the left ventriculogram done with amyl nitrite and Valsalva, left ventricular volumes in both decreased dramatically, from 69 ml/m2 to 43 ml/m2 (p less than 0.001) and ejection fraction increased from 70% to 82% in group A (p less than 0.01). None of the patients in group A had evidence of cavitary obliteration at rest, but eight developed total and two developed partial cavitary obliteration with the second ventriculogram. Three patients in group B had partial or complete cavitary emptying at rest and all developed total cavitary obliteration with provocation. Pressure gradients between left ventricle and aorta were produced in two group A patients and three group B patients. Thus, cavitary obliteration can be produced in normal left ventricles by manipulation of loading conditions.

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