Patients In Group IA Research Articles

Sarcoidosis of the heart: A clinicopathologic study of 35 necropsy patients (group I) and review of 78 previously described necropsy patients (group II)

Certain clinical and morphologic observations are described in 35 necropsy patients with cardiac sarcoidosis (group IA and IB), and similar observations are summarized in 78 previously described necropsy patients with cardiac sarcoidosis (group IIA and IIB). All patients had non-necrotic (“hard”) granulomas in lymph nodes and either sarcoid granulomas in the heart (108 patients) or transmural myocardial scarring (five patients) unassociated with coronary arterial narrowing, i.e., healed granulomas. The 113 patients (groups I and II) whose data are analyzed also were divided into those in whom cardiac dysfunction clearly was the result of sarcoid granulomatous infiltration of the heart (89 patients) (groups IA and IIA), and those in whom cardiac dysfunction, if present, was clearly not the result of sarcoid involvement of the heart (24 patients) (groups IB and IIB). Analysis of the 89 patients in groups IA and IIA disclosed that death was sudden (arrhythmia) in 60 (67 per cent), secondary to progressive congestive cardiac failure in 20 (23 per cent), from recurring pericardial effusion in three (3 per cent) and from other or unknown causes in six (7 per cent). Sudden death was the initial manifestation of sarcoidosis in 10 (17 per cent) of the 60 patients who died suddenly. Other than premature ventricular beats, ventricular tachycardia was the most common arrhythmia (17 patients), and complete heart block was the most common conduction disturbance (25 patients). Complete bundle branch block occurred in 21 patients. Ventricular aneurysm (eight patients) and papillary muscle dysfunction (possibly 16 patients) were other cardiac disturbances observed. Although corticosteroid therapy tends to cause fibrous replacement of myocardial sarcoid granulomas, a possible consequence of this medication is the development of ventricular aneurysm. Most patients with cardiac sarcoidosis causing dysfunction (groups IA and IIA) presented initially with manifestations related to the heart. Furthermore, most patients with cardiac sarcoidosis have little or no clinical evidence of dysfunction of an organ system other than the heart. Usually the course in patients with extensive cardiac sarcoidosis is not prolonged.

Comparative study of exercise-induced ventricular arrhythmias in normal subjects and patients with documented coronary artery disease

The incidence, types and patterns of emergence of treadmill exercise-induced ventricular arrhythmias were studied in 482 subjects with and without coronary heart disease. All subjects were free of premature ventricular complexes at rest and were classified into groups on the basis of their clinical status. In Group IA were 141 patients with chest pain and normal coronary arteriograms and in Group IB 144 age-matched subjects free of clinical evidence of heart disease. Group II consisted of 197 patients with chest pain and arteriographically documented coronary artery disease. Patients in Group IA and II exercised to at least 85 percent of their predicted maximal heart rate or until chest pain occurred. Subjects in Group IB underwent maximal exercise testing. The total incidence of exercise-induced ventricular arrhythmias was 16 percent in Group IA, 44 percent in Group IB and 29 percent in Group II. However, when exercise heart rate at the time of appearance of ventricular arrhythmias was taken into account the incidence of exercise-induced ventricular arrhythmias up to a heart rate of 130/min was 27 percent in the patients with documented coronary artery disease (Group II) compared with rates of 9 and 6 percent, respectively, for Groups IA and IB ( P < 0.001). The incidence rates of multifocal ventricular premature complexes, ventricular tachycardia and ventricular premature complexes at a rate of more than 10/min were also significantly greater at submaximal heart rates in the patients with coronary disease. Patients with three vessel coronary artery disease and abnormal left ventricular wall motion had a significantly greater incidence of exercise-induced ventricular arrhythmias. The incidence of exercise-induced ventricular arrhythmias in patients with coronary disease and a positive S-T segment response was not significantly increased.

Acute Mitral Regurgitation Resulting from Ruptured or Elongated Chordae Tendineae&lt;subtitle&gt;AUSCULTATORY AND PHONOCARDIOGRAPHIC FINDINGS&lt;/subtitle&gt;

Eighteen patients with severe acute mitral regurgitation requiring operation have been described. The history, physical signs and phonocardiographic findings were compared with the anatomical findings at operation. Fourteen had ruptured chordae tendineae (five anterior leaflet: eight posterior leaflet: one both leaflets) and four had elongated chordae with prolapsing leaflets. The commonest auscultatory finding was an apical pan-systolic murmur with a mid-systolic crescendo which was often propagated to the base and into the neck thus simulating aortic stenosis. The mid-systolic crescendo appeared to be due to the regurgitant flow of a high velocity jet through a relatively small regurgitant orifice. The basal propagation was due to the regurgitant jet being directed forwards and medially against the atrial septum in the region of the aortic root. This type of murmur was found in patients with either anterior or posterior leaflet chordal rupture and also in some patients with elongated chordae. It was therefore of no help in differentiating these lesions. A plateau shaped pan-systolic murmur was never found in patients with ruptured chordae to the posterior leaflet. A loud first heart sound was often present particularly in the presence of an intact anterior leaflet. All patients had third heart sounds and all but one of those in sinus rhythm had an atrial sound which was often associated with a palpable atrial impulse and a tall ‘A’ wave on the apexcardiogram. The clinical findings therefore did not readily distinguish between the different groups of patients. Left ventricular cine-angiography was the best method of determining the site of leaflet prolapse. Although an underlying cause was found for ruptured chordae in most of the Group IA patients, the aetiology was obscure in the remainder. The Group II patients with elongated chordae and voluminous leaflets clearly had degeneration of the valve tissues but whether this was acquired or due to an inherited anomaly remains unknown.