Heart

Murray, R G; Tweddel, A; Third, J L; Hutton, I; Hillis, W S; Lorimer, A R; Lawrie, T D

doi: 10.1136/hrt.37.12.1205pmid: 178330

Lipoprotein analyses were performed in 133 male patients and were correlated with the coronary arteriographic findings. The prevalence of hyperlipoproteinaemia was significantly higher in those patients with coronary artery disease (P less than 0-02). In addition, the more extensive the degree of coronary artery pathology the higher were the plasma concentrations of total cholesterol, triglyceride, and low density lipoprotein (LDL) cholesterol. Hyperlipoproteinaemia was more prevalent in the younger patients with coronary artery disease (P less than 0-02).

Bulpitt, C J

doi: 10.1136/hrt.37.12.1210pmid: 1225335

Both the average serum uric acid and annual increment were determined in 250 treated patients attending a hypertension clinic. The average serum uric acid was greater in men compared with women, in patients receiving a thiazide diuretic and in patients with a high average plasma urea. The mean annual increment in uric acid was close to zero (0.0017 mmol/litre per year) and was not related to sex, age, blood pressure control, diuretic therapy, or plasma urea. There was an unexplained positive association between annual increment and methyldopa therapy though this drug was not associated with a significantly high average serum uric acid. A table is presented giving the theoretical upper limits for average serum uric acid according to sex, plasma urea concentration, and whether or not a thiazide diuretic has been prescribed. It is hoped that this table will be of assistance in assessing the normality or otherwise of a high serum uric acid found in a hypertensive patient.

Neuss, H; Schlepper, M; Spies, H F

doi: 10.1136/hrt.37.12.1216pmid: 1225336

In patients with evidence of dual AV conduction, a premature atrial depolarization is normally conducted via a fast conducting pathway with a long refractory period. At a critically timed coupling interval, the effective refractory period is reached and now the impulse is conducted over a pathway with a slow conduction velocity and a short effective refractory period. At this moment in the His bundle electrocardiogram, a sudden increase in the AH interval occurs which is called the 'break' phenomenon. This phenomenon was studied in 14 patients, with a history of supraventricular paroxysmal tachycardia, at the patient's own heart rate, at different paced heart rates, and after the administration of atropine. In 11 patients the 'break' phenomenon could be elicited during sinus rhythm,; in 3 when the heart rate was accelerated. The effective refractory period of the fast conducting pathway was prolonged in 9 patients, remained unchanged in 3, and was shortened in 2 when the heart rate was increased. The effective refractory period of the slow conduting pathway was reached when block occurred proximal to the His bundle. This parameter was increased in 8 patients, remained unchanged in 3, and was decreased in 1 patient with augmentation of the heart rate. This effective refractory period was not measured in 2 patients. Atropine led to a shortening of the refractory period of both pathways in 8 patients studied. Atrial echo phenomena indicating the beginning of a re-entry circuit occurred at an AH prolongation that was not always identical to that measured at the point of 'break'. Widening, as well as narrowing, of the echo zone was found, indicating that the re-entry circuit was in a state of labile equilibrium. In cases where shortening of the pathways involved in the re-entry circuit was found, structures other than nodal may exist; therefore paranodal bypass must be considered.

Coltart, D J; Cayen, M N; Stinson, E B; Goldman, R H; Davies, R O; Harrison, D C

doi: 10.1136/hrt.37.12.1228pmid: 1225337

The time necessary for dissipation of radioactive labelled propranolol and its metabolites and the cardiac effects of this agent in the hearts of patients undergoing open-heart surgery were studied. Isoprenaline produced chronotropic and inotropic responses in atrial muscle in tissue bath studies which were normal 8 to 12 hours after withdrawing propranolol. After the administration of either 25 or 75 muCi of 14C-labelled propranolol, the myocardial tissue concentration declined to insignificant levels between 24 and 28 hours. We conclude that withdrawal of propranolol therapy 24 to 48 hours before cardiac surgery should be acceptable.

Guazzi, M; Fiorentini, C; Polese, A; Magrini, F; Olivari, M T

doi: 10.1136/hrt.37.12.1235pmid: 773391

Propranolol and practolol were tested in patients with repeated daily occurrence of spontaneous angina. Twenty-one showed ST segment depression (type I) and 15 ST segment elevation (type II) during angina. The efficacy of the treatment was evaluated in subjective (number of reported episodes of pain) and objective terms (number of episodes of electrocardiographic abnormalities documented during periods of continuous recording): practolol was fully effective in 42 per cent and propranolol in 38 per cent of type I cases; in type II angina 73 per cent of the cases fully responded to propranolol, none of the patients in this group given practolol improved. The study also showed that: (a) the effects on angina are strictly dose-dependent, and optimal results are achieved at individualized doses; (b) within the same subject the response may be preferential to one beta-blocker as opposed to the other; (c) propranolol is more effective in type II angina; (d) the occurrence of heart failure is uncommon even with high doses of beta blockers;(e) the relief of angina is due to prevention of ischaemia and not to a placebo or anaesthetic effect; (f) the prevention of ischaemia is not adequately explained by reduction of the mechanical effort and the oxygen need of the myocardium; (g) the antianginal effect is possibly dissociated from the beta blockade of the heart. The hypothesis that beta-blocking agents influence the conronary vasomotion is discussed.

Chahine, R A

doi: 10.1136/hrt.37.12.1246pmid: 1225338

Unstable angina is used interchangeably with a variety of other terms to refer to a clinical situation intermediate in severity between chronic effort angina and myocardial infarction. In most reports dealing with this syndrome, the patients were selected according to a number of criteria which varied from one study to another. Some authors recognized subgroups of patients with variable severity while others looked at unstable angina as one single group. This resulted in conflicting observations and consequent dilemmas in the management of these patients. Accurate definitions are, therefore, necessary. It is proposed to divide unstable angina into two main clinical categories. Type I: This includes three subgroups. (A) Patients with known chronic angina and sudden or accelerated progression of symptoms; (B) patients with chronic angina and onset of recurrent attacks at rest; and (C) patients with angina of recent onset and rapid progression into a severe condition. Type II: (severe unstable angima). Any of the subgroups described under unstable angina Type I will qualify for this classification if the patient develops recurrent episodes of prolonged ischaemic chest pains resistant to nitroglycerin lasting for 15 minutes or more. Accurate measurement of symptoms and laboratory criteria are suggested to qualify for the different subgroups of unstable angina.

Fuster, V; Frye, R L; Connolly, D C; Danielson, M A; Elveback, L R; Kurland, L T

doi: 10.1136/hrt.37.12.1250pmid: 1225339

Coronary arteriography in 300 patients within one year of onset of symptoms of coronary arterial disease revealed already severe anatomical coronary disease in three patient groups: those with angina pectoris alone (164 patients), with subendocardial myocardial infarction (63 patients), and with transmural myocardial infarction (73 patients). The number of vessels diseased (larger than or equal to 50% obstruction), distribution of obstruction, and degree of stenosis were similar in the three groups. However, total occlusion of at least one artery was much more common in transmural myocardial infarction and in subendocardial myocardial infarction with elevation of enzyme levels. We suggest that such occlusions occurred at the time of the infarction. Similarities in coronary anatomy between patient subgroups with angina (on exercise or at rest and nocturnal) indicate that factors other than coronary anatomy intervene in precipitating the different types of angina. Vessel disease was not related to smoking, hyperlipidaemia, or hypertension but coronary disease was manifest earlier in life in smokers or those with hyperlipidaemia.

Prewitt, T; Gibson, D; Brown, D; Sutton, G

doi: 10.1136/hrt.37.12.1256pmid: 1225340

In order to study the relation between the 'rapid filling wave' of the apex cardiogram and left ventricular filling, simultaneous apex cardiograms, phonocardiograms, and echocardiograms were recorded in 57 patients. Continuous measurements of left ventricular dimension were derived from the echocardiograms by digitization using manual tracing and a computer. Possible errors in the use of a single dimension to assess left ventricular filling were investigated by frame-by-frame analysis of cineangiocardiograms in 37 patients, and the timing of changes in transverse diameter found to correlate closely with those in cavity area. Mitral valve opening, shown as the initial separation of the valve cusps by echocardiography, preceded the 'O' point of the apex cardiogram in all except 3 patients, the 'O' point appearing to correlate more closely with the time of peak rate of outward wall movement. A third heart sound was present in 29 patients, and in 25 of these it occurred later than the peak rate of wall movement (ment interval 51 ms). The end of rapid filling derived from the dimension trace occurred in relation to the third heart sound after a mean interval of 9 ms, with a range from 50 ms before to 80 ms after the third sound. Peak rates of wall movement were similar in patients with and without third heart sounds. The results show that outward left ventricular wall movement begins with a period of acceleration, with peak rates occurring synchronous with the 'O' point of the apex cardiogram and thus with the nadir of the ventricular pressure trace. Outward wall movement becomes less rapid thereafter, so that the rapid filling wave of the apex cardiogram does not reflect the time of rapid filling of the left ventricle. The 'O' point is not related to mitral valve movement nor does the third heart sound bear a consitent relation to any aspect of left ventricular wall movement.

Manolas, J; Rutishauser, W; Wirz, P; Arbenz, U

doi: 10.1136/hrt.37.12.1263pmid: 1225341

In 10 patients without left heart valvular disease and having normal function of the left ventricle, the left ventricular apex cardiogram with its first derivative (dA/dt), left ventricular pressure with its first derivative (dP/dt), aortic pressure, electrocardiogram, and phonocardiogram were reocrded simultaneously during cardiac catheterization. The apex cardiographic tracings were obtained by means of a transducer with infinite time constant and very high resonant frequency and the LV and aortic pressures with catheter tip-manometers. The onset of the systolic rise of apex cardiographic and LV pressures were found to occur almost simultaneously with the upstroke of LV pressure, preceding that of the apex cardiogram by only 2 +/- 4 ms (mean +/- 1 SD). The summit of the systolic upstroke of the apex cardiogram (called E-point) occurred 37 +/- 9 ms after opening of the aortic valve and 41 +/- 9 ms after peak dP/dt. The peak of dA/dt preceded peak dP/dt by 10 +/- 4 ms. The protodiastolic nadir of the apex cardiogram (called-O-point) occurred slightly earlier (19 +/- 16 ms) than the nadir of the LV pressure curve, with considerable variation. In conclusion, this study using external and internal transducers with similar characteristics gives a new definition of the time relation between the externally recorded apex cardiogram and the haemodynamic events within the left heart in human subjects with normal left ventricular function.

Thiene, G; Cucchini, F; Pellegrino, P A

doi: 10.1136/hrt.37.12.1268pmid: 1225342

Two cases are reported of truncus arteriosus communis arising entirely from the right ventricle and associated with interruption in one case and tubular hypoplasia of the aortic arch in the other. A haemodynamic hypothesis of preferential blood flow is proposed to explain this rare association.