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Biomedical subjects

H O Hirzel

Publications and source records attributed to H O Hirzel.

At least 37 records · Page 2Linked to original sources
PubMed1985

[Drug treatment of hypertrophic cardiomyopathy].

Both, beta-receptor blocking agents and calcium-antagonists have been proven to be very effective in the treatment of idiopathic hypertrophic cardiomyopathy. In the vast majority of patients they lead to a significant reduction of the predominant clinical symptoms--angina and dyspnea--or even abolish them. Since beta-blockers primarily act on the contractile behaviour of the left ventricle they are especially suited in the obstructive form of the disease where they reduce outflow tract obstruction. In contrast, calcium-antagonists seem to mainly influence diastolic muscle mechanics by increasing diastolic distensibility, and thus may be indicated in the nonobstructive forms of hypertrophic cardiomyopathy. In cases with severe, life-threatening arrhythmias especially if associated with syncope, an antiarrhythmic therapy is mandatory.

Anti-Arrhythmia Agents↗
PubMed1984

Thallium-201 scintigraphy in complete left bundle branch block.

Nineteen symptomatic patients with left bundle branch block (LBBB) were examined by thallium-201 (TI-201) exercise scintigraphy and selective coronary arteriography. All elicited significant anteroseptal perfusion defects in the exercise scintigrams, but in only 4 was coronary artery disease (CAD) involving the left anterior descending coronary artery present. To further elucidate the effect of LBBB on septal TI-201 uptake in the absence of CAD, TI-201 scintigrams combined with regional myocardial blood flow measurements using radioactive microspheres were carried out in 7 dogs during right atrial and right ventricular pacing (LBBB in the ECG) at similar heart rates. During right atrial pacing, TI-201 uptake was homogeneous in the entire left ventricle, as were tissue flows. During right ventricular pacing, TI-201 activity was reduced to 69% of maximal TI-201 activity within the septum, whereas it averaged 90% in the lateral wall (p less than 0.05) in 6 dogs. Correspondingly, regional myocardial blood flow was lower within the septum as compared with that in the lateral wall, averaging 89 and 120 ml/min/100 g, respectively (p less than 0.005). In 1 dog, normal TI-201 distribution and tissue flows were found in both studies. Thus, symptomatic patients with LBBB may elicit abnormal TI-201 exercise scintigrams, suggesting anteroseptal ischemia despite normal coronary arteries. The electrical induction of LBBB in dogs results, in most instances, in a comparable reduction in septal TI-201 uptake associated with diminished septal blood flow. Therefore, exercise-induced septal perfusion defects in the presence of LBBB do not necessarily indicate CAD even in symptomatic patients, but may reflect functional ischemia due to asynchronous septal contraction.

Adult↗
PubMed1984

Myosin isoenzymes in human hypertrophic hearts. Shift in atrial myosin heavy chains and in ventricular myosin light chains.

The myosin light chain complement and proteolytic peptide patterns of myosin heavy chains were studied by two-dimensional and one-dimensional electrophoretic techniques respectively, in a total of 57 samples from ventricular and atrial tissues of normal and hypertrophied human hearts. Hypertrophies were classified haemodynamically as due to pressure-overload and volume-overload. In addition to the occurrence of ventricular light chains in hypertrophied atria we also observed the atrial light chain-1 (ALC-1) in hypertrophied ventricular tissues. On average over 6% of total light-chain-1 comprised ALC-1 in pressure-overloaded ventricles and around 3% in volume-overloaded ventricles. In single cases of pressure-overload ALC-1 amounted up to over 20% of total light chain-1. With regard to the myosin heavy chains limited digestion by two different proteinases produced over 200 clearly resoluble peptides. The absence of any detectable differences in the peptide patterns between myosin heavy chains from normal and hypertrophic tissues of left or right ventricle is in line with the findings of J. J. Schier and R. S. Adelstein (J Clin Invest 1982; 69: 816-825). In atrial tissues however, reproducible qualitative differences in the peptide patterns indicated that during hypertrophy a different type of myosin heavy chains becomes expressed. No differences were seen between the myosin heavy chains from normal left and right atria.

Cardiomegaly↗
PubMed1984

[Hemodynamics in ischemia. Systolic phase].

Experimental animal investigations have shown that already after a few seconds of occlusion of a coronary artery a reduction in the systolic myocardial shortening and wall thickening takes place in the corresponding supply area. Following 1-2 minutes of ischemia systolic expansion occurs. Wall-thickness increase and myocardial shortening then take place during the isovolumetric relaxation phase. When at least 25% of the myocardium of the left ventricle becomes acutely ischemic the end-diastolic pressure and end-diastolic volume increase. As a rule an augmentation of myocardial contraction appears in the non-ischemic section of myocardium, which in part takes place through the Frank-Starling mechanism. With a gradual reduction of the coronary inflow, and a decline in the wall thickening of c. 50% of the control value, a significant reduction in blood flow took place only in the innermost quarter of the ventricular wall. With akinesia of the ischemic area, no reduction of the blood flow could be determined in the subepicardial region. Only with the occurrence of dyskinetic wall motion was a transmural reduction of blood flow effected. The ischemic contraction disturbances are fully reversible if coronary occlusion last only a few minutes. With a 15 minute occlusion the recovery time of the myocardial function can require several days (postischemic "stunned myocardium"). The first myocardial necroses occur after 20 minutes of ischemia, and after 3-6 hours of ischemia the infarction is complete.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1983

Systolic function during exercise in patients with coronary artery disease.

Global and regional systolic function during exercise were studied at cardiac catheterization with biplane cineangiography and micromanometer pressures in three groups of patients: an ischemia group (n = 22) with exercise-induced asynergy from coronary artery disease, a control group with no or minimal cardiovascular disease (n = 5) and a "scar" group (n = 5) with prior infarction and no new asynergy with exercise. Ventricular emptying curves at rest did not distinguish patients with coronary artery disease from control subjects. During exercise, end-systolic volume increased in all patients in the ischemia group; ejection fraction decreased from 62 to 51% p less than 0.001) despite an increased end-diastolic volume. Stroke volume decreased from 65 to 58 ml/m2 (p less than 0.001) and limited the average increase in cardiac index to 65%. The scar group had no decrease in stroke volume, but end-systolic volume failed to decrease during exercise, as it did in all control subjects (35 to 28 ml/m2, p less than 0.05). An exercise-induced decrease in peak left ventricular pressure in five patients (23%) in the ischemia group was not accompanied by more severe or extensive ischemia as judged by ejection phase indexes. There was a tendency for maximal positive first derivative of left ventricular pressure (dP/dt) to be less (1,912 versus 2,446 mm Hg/s, difference not significant), suggesting an abnormality of pressure generation, not shortening. Global function during exercise in the ischemia group was determined, in part, by the extent of regional dysfunction. Those in whom between three and five regions of eight regions studied had abnormal fractional shortening during exercise had a 6% decrease in ejection fraction, while those with six to eight abnormal regions had a decrease in ejection fraction of 15% (p less than 0.05). In addition, function of nonischemic, noninfarcted myocardium was studied at the base of the left ventricle in those with exercise-induced anteroapical ischemia (n = 4) and those with anteroapical infarction (n = 4). Base fractional shortening and shortening velocity were greater at rest in those with infarction (39% and 1.6 circ/s, respectively) than in control subjects (31% and 1.0 circ/s, respectively, p less than 0.01), indicating a chronic augmentation of shortening. Base shortening velocity during exercise in those developing anteroapical ischemia increased from 1.1 to 1.4 circ/s (p less than 0.005), suggesting an acute augmentation of function balancing the deterioration of anteroapical function. Systolic function in coronary artery disease is determined by acute and chronic alterations in regional function. During exercise, there is an interplay between regional dysfunction from ischemia or infarction and regional hyperfunction of nonischemic myocardium which determines global performance.

Adult↗
PubMed1983

Exercise-induced ischemia: the influence of altered relaxation on early diastolic pressures.

Left ventricular pressure (LVP) decay and early diastolic pressures were studied at rest and during exercise in three groups of patients. Patients in the ischemia group (n = 15) had coronary artery disease and developed new regional wall motion abnormalities documented by biplane LV cineangiography during exercise. Patients in the control group (n = 4) had a normal exercise response. Patients in the scar group (n = 5) had prior infarction, akinetic scars and no ischemia with exercise. Isovolumic pressure data were used to compute the time constant (T) of LVP decay (from the linear relation of LVP and negative dP/dt) and an extrapolated baseline pressure (PB) at dP/dt = 0. During exercise in the ischemia group, minimal LV diastolic pressure (PL) increased from 9 +/- 3 to 21 +/- 5 mm Hg (p less than 0.001), end-systolic volume increased from 38 +/- 7 to 55 +/- 8 ml/m2 (p less than 0.001) and PB rose from -10 +/- 7 to 11 +/- 8 mm Hg (p less than 0.001); T decreased (from 55 +/- 9 to 37 +/- 8 msec, p less than 0.001), although inadequately, compared with the decrease in the control group (from 49 +/- 15 to 22 +/- 2 msec, p less than 0.01). Relaxation at PL during exercise was incomplete in the ischemia group (2.2 +/- 0.4 T) and complete in the control group (3.8 +/- 0.7 T, p less than 0.05). The time course of LVP fall was extrapolated from the isovolumic period into the passive LV filling phase. The extrapolated pressure at the time PL occurred (PE) rose from 0 +/- 4 to 20 +/- 7 mm Hg with ischemia (p less than 0.001). Thus, the characteristics of LVP decay can account for the elevated early diastolic pressures during ischemia. In contrast, the scar group maintained a low PL during exercise (11 +/- 3 to 8 +/- 3 mm Hg), even though T decreased inadequately (from 66 +/- 10 to 36 +/- 5 msec, p less than 0.01), because PB did not shift upward. Ischemia-related pressure elevations involve both delayed relaxation and a pressure baseline shift. During exercise, LVP decay is normally adjusted to maintain low diastolic pressures; with exercise-induced ischemia, LVP decay is abnormal and early diastolic pressures are severely elevated.

Adult↗
PubMed1983

Dynamics of left ventricular filling at rest and during exercise.

Left ventricular filling dynamics were examined at rest and during supine bicycle exercise in 33 patients at cardiac catheterization; 23 had coronary artery disease (ischemia group), five with prior infarction had an akinetic area at rest (scar group), and five had minimal cardiovascular disease (control). Peak filling rate and mean filling rate during the first half and second half of diastole were assessed by biplane angiography. Simultaneous micromanometer pressures were used to compute the time constant of isovolumic pressure decay (T). Peak filling rate and mean filling rate during the first half of diastole increased with exercise in all groups (from 615 to 1050 and 358 to 681 ml/sec in controls and comparably in the scar group and from 697 to 1035 and 347 to 768 ml/sec in the ischemia group). However, T was greater (reduced rate of pressure decay) with exercise in the ischemia group (38 vs 26 msec in controls; p less than .05). Changes in the atrial driving pressure for filling appeared to counterbalance the difference in T. Mean filling rate during the second half of diastole increased with exercise in controls and in the scar group but only modestly in the ischemia group (from 202 to 349 ml/sec). The reduction in late diastolic filling during exercise-induced ischemia was associated with increased filling in early diastole, with a middiastolic volume increase from 160 to 186 ml and an upward shift in the diastolic pressure-volume relation. Thus left ventricular filling is not impaired at rest in patients with coronary artery disease who have normal ejection fractions. Furthermore, the augmentation of early filling induced by exercise is not blunted but is maintained during ischemia, apparently at the expense of elevated left atrial pressure. However, late filling is restricted with ischemia by an increase in impedance.

Cardiac Catheterization↗
PubMed1983

Does isosorbide-5-mononitrate influence left ventricular relaxation?

In 25 patients, 21 of whom had coronary heart disease, left ventricular high-fidelity pressure measurements, M-mode-echocardiograms, phono- and electrocardiograms were carried out before and 20 min after peroral administration of 50 mg isosorbide-5-mononitrate. Left ventricular relaxation was assessed by the isovolumic relaxation time, left ventricular max negative dP/dt, the time constant, T, of left ventricular pressure decay during the isovolumic relaxation period, and peak fall of meridional wall stress (max negative dS/dt). Following isosorbide-5-mononitrate the heart rate was not altered; left ventricular systolic pressure, however, decreased from 129 to 117 mmHg (P less than 0.001) as did the end-diastolic pressure from 15 to 8 mmHg (P less than 0.001). The left ventricular end-diastolic diameter decreased from 53 to 50 mm (P less than 0.001) and left ventricular peak stress from 182 to 142 X 10(3) dynes/cm2 (P less than 0.001). Max dP/dt and left ventricular systolic shortening remained essentially unchanged, indicating that contractility during the isovolumic-contraction phase as well as during ejection was not influenced. Max negative dP/dt, max negative dS/dt, and the isovolumic relaxation time also remained unchanged. T, however, decreased from 54 to 45 ms (P less than 0.001). We conclude that peroral administration of isosorbide-5-mononitrate is followed by a decrease in pre- and afterload, but also by an increase in the speed of left ventricular relaxation as evidenced by the diminished T. Since T has been reported as being load-independent, its decrease either reflects a genuine effect of isosorbide-5-mononitrate on left ventricular relaxation or results from a diminution of residual ischemia.

Adult↗
PubMed1982

[Is the aorto-coronary bypass operation useful in patients with advanced coronary sclerosis and poor ventricular function?].

The prognosis and long term results in 56 patients with coronary artery disease and impaired left ventricular function (EF less than or equal to 40%) who underwent aortocoronary bypass surgery (all cases) and aneurysmectomy (26 cases) between 1972 and 1980 were compared with those in 47 equally ill patients treated medically. Survival was significantly higher in the surgical than in the non-surgical group, the survival rate being 80% and 58% respectively at 41 months after study entry (p = 0.012). No difference in survival was observed between grafted patients and patients in whom additional aneurysmectomy was performed. 26 patients were recatheterized postoperatively and this revealed an increase in left ventricular ejection fraction at rest from 33 +/- 5% to 44 +/- 11% (p less than 0.001) and a decrease in left ventricular end-diastolic pressure from 18 +/- 8 mm Hg to 14 +/- 8 mm Hg (p less than 0.025). Postoperatively the patients had less angina and physical working capacity increased. At restudy the average NYHA class had decreased in the surgical group from 2.9 +/- 0.7 to 2.1 +/- 0.9 (p less than 0.001) but was unchanged in the non-surgical group (2.6 +/- 0.6 and 2.6 +/- 0.7 respectively). It is concluded that aortocoronary bypass surgery improves survival, left ventricular function and symptoms in patients with coronary artery disease and severely impaired myocardial function.

Adult↗
PubMed1982

[Etiology and clinical course of bacterial endocarditis, 1971-1980].

Etiology and clinical course of infective endocarditis were analyzed in 31 patients seen at this institution between 1971 and 1980. The follow-up period averaged 60 (1-180) months. The infection relapsed 9 times (relapse rate 31-38%). The etiologic agent isolated from blood cultures in 26/42 infective episodes. Penicillin-sensitive streptococci were by far the most frequent cause of infective endocarditis (46%), followed by Staphylococcus aureus in 23%. A predisposing cardiac lesion existed in 26/31 patients (84%), aortic valve disease and a prolapsing mitral valve being the most frequent. In the 31 patients there were 5 deaths, 2 of which occurred acutely within a few days following the onset of endocarditis (mortality rate 6%), 2 suddenly after completion of antimicrobial therapy and 1 from another cause during the observation period. Surgery was necessary in 18 patients, emergency valve replacement being required in 3 cases (10%). In 15 patients (52%) cardiac surgery was performed electively after healing of the endocarditis. The indication for surgery was onset of heart failure due to valvular incompetence in 16 patients and recurrent systemic embolization in 2 patients. All patients survived surgery. At restudy no difference was observed in overall cardiac function, physical working capacity and employment activities among the surviving patients whether operated upon or not.

Adolescent↗
PubMed1982

[Function of the left ventricle under dynamic load in patients with coronary heart disease with and without angina pectoris].

Overall left ventricular function and regional wall motion abnormalities visualized by biplane cineangiocardiography were examined in 136 patients with significant coronary heart disease during supine bicycle ergometry. The stress test was tolerated without symptoms in 57 patients (42%) (26 without previous myocardial infarction, 31 with infarction), whereas it was limited by angina pectoris in 79 (58%) (40 without previous infarction, 39 with infarction). A de novo asynergy during exercise was observed in a similar percentage in patients without angina (17/26 [65%] without infarction, 29/31 [94%] with infarction) than in those with angina (29/40 [73%] without infarction, 33/39 [85%] with infarction). During exercise, left ventricular ejection fraction decreased and enddiastolic pressure increased to the same extent in all four subgroups, all changes being highly significant. It is concluded that in patients with coronary heart disease objective signs of ischemia during exercise (de novo asynergy, fall in ejection fraction and rise in enddiastolic pressure) are observed independently of whether angina pectoris occurred or not. Thus, angina is not an indispensable symptom of the occurrence of hemodynamically relevant ischemia during dynamic exercise.

Adult↗
PubMed1982

[Prognosis and clinical course in patients with advanced, inoperable coronary heart disease].

The clinical course, factors of prognostic significance and the quality of life in 128 patients with coronary heart disease rejected for revascularization surgery between 1970 and 1981 and followed up for 1-135 months (mean 43 months) were evaluated. The reason for rejection for bypass surgery was poor left ventricular function in 15 patients, diffusely diseased coronaries in 82 patients and both of the above in 31 patients. The actuarial 5-year survival rate in the entire population amounted to 53%, resulting in an average annual mortality rate of 9.4%. Left ventricular ejection fraction and end-diastolic pressure at rest were the only parameters of prognostic significance. Neither age, history of myocardial infarction, physical working capacity nor the number of diseased vessels were of prognostic value. Despite having "inoperable" coronary artery disease, many patients were able to continue gainful employment (61%) and were not severely restricted by angina (50% NYHC I-II).

Adult↗
PubMed1982

[Calcium antagonists in the treatment of heart diseases].

The beneficial action of calcium antagonists in the therapy of different cardiac diseases is based on one fundamental effect, i.e. reduction of the transmembrane calcium conductivity of myocardial muscle fibers and vascular smooth musculature. The pharmacologic effects of calcium antagonists can be summarized as follows: 1. The myocardium shows a reduction in oxygen consumption due to the decrease in systolic wall stress and depression of myocardial metabolism. 2. Pacemaker activity and AV-node conduction are depressed, while ectopic pacemaker activities are effectively suppressed and reentry mechanisms are blocked. 3. The vascular smooth musculature shows a reduction of vascular tone and suppression of arterial spasms. The clinical use of calcium antagonists is based on the following four important therapeutic factors: 1. antianginal effect, 2. antiarrhythmic effect, 3. antihypertensive effect, 4. cardioprotective effect. Currently the calcium antagonists are used mainly in the treatment of supraventricular tachyarrhythmias and coronary vasospasms. New fields for calcium blockers may be therapy of hypertrophic cardiomyopathy and myocardial protection during acute myocardial ischemia.

Calcium Channel Blockers↗
PubMed1982

Electrophoretic analyses of atrial and ventricular cardiac myosins from foetal and adult rabbits.

1. Rabbit cardiac myosins from atrium and ventricle were found to differ in their native form in pyrophosphate gel electrophoresis as well as in their light chain pattern in one- and two-dimensional electrophoretic systems. 2. The myosin light chain pattern in sodium dodecylsulfate gel electrophoresis differs between atrial and ventricular tissues in the mammalians (rabbit, dog, human, pig, sheep and rat) but not in the chicken. 3. In foetal rabbit ventricle an additional light chain is observed which, in two-dimensional electrophoresis with adult cardiac light chains, was found to be the same as atrial light chain-1.

Animals↗