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Biomedical subjects

M Kaltenbach

Publications and source records attributed to M Kaltenbach.

At least 325 records · Page 18Linked to original sources

Reduction of CK and CK-MB indexes of infarct size by intravenous nitroglycerin.

The effect of i.v. nitroglycerin administration on indexes of infarct size was examined in 31 patients with acute myocardial infarction. Serial creatine kinase (CK) and CK-MB isoenzyme determinations were used to calculate infarct size. Twenty-nine patients served as controls. Two subgroups of the study group were formed to evaluate differences between early and late intervention. In the first group (n = 22), continuous infusion of nitroglycerin over 48 hours was initiated within 8 hours (mean 4.5 hours) after the onset of symptoms. Peak CK activity for the nitroglycerin-treated patients (n = 9) in this subgroup was 544 U/1 vs 871 U/1 for the controls (n = 13) (p less than 0.05). The rate of CK release was reduced from 79 to 33 U/1.hr (58%), as was total CK and CK-MB release (p less than 0.02). Calculated infarct size was 69 gEq in the controls and 48 gEq in patients receiving nitroglycerin (CK-MB: 69 vs 43 gEq, p less than 0.05). In the late intervention subgroup, nitroglycerin therapy was begun more than 8 hours (mean 12.8 hours) after the onset of symptoms. Here, too, use of the agent was associated with lower peak CK and CK-MB levels as well as a reduction in calculated infarct size (p less than 0.05). Hemodynamic measurements, recorded every 4 hours, showed that nitroglycerin also reduced left ventricular filling pressure significantly and cardiac output increased. Blood pressure fell slightly, and systemic vascular resistance declined. The results indicate that i.v. nitroglycerin reduces CK and CK-MB release and thus calculated infarct size in both early and late intervention.

Adult↗

[Changes in diameters of small pulmonary venous and arterial vessels after nitroglycerin (author's transl)].

Diameters of the small arterial and venous pulmonary vessels were studied in 17 patients, using selective pulmonary angiography. The majority had coronary heart disease. Pulmonary and systemic hemodynamics were also evaluated. In 11 patients, these procedures were repeated 3 minutes after the sublingual administration of 1.6 mg of nitroglycerin (Group I). The remaining 6 patients served as controls (Group II). In Group I, pulmonary circulatory pressures, left ventricular filling pressure, and pulmonary vascular resistance declined significantly compared with Group II. The diameters of the small pulmonary veins declined by more than 10 percent in Group I while remaining constant in Group II. Differences between the two groups in terms of the response of the small arterial vessels was less evident. Increases in vessel cross-sectional area were observed despite considerably reduced intravascular pressure. The increase in elasticity and capacitance of the pulmonary vessels following nitroglycerin is more pronounced on the venous than on the arterial side. These findings suggest that the pulmonary vascular bed contributes significantly to the therapeutically important pooling effect caused by nitroglycerin in the treatment of angina pectoris and pulmonary edema.

Coronary Disease↗

[Improved myocardial function after transluminal coronary angioplasty (author's transl)].

To assess the results of transluminal coronary angioplasty (TCA), 42 patients (mean age 50 years) with for coronary artery disease were investigated at rest and during exercise with the ECG (n = 40), thallium-201 myocardial scintigraphy (n = 23) and equilibrium-radionuclide ventriculography (n = 32). Each method of stress testing was quantified: the exercise ECG by means of an ischemia score, incremented with increasing ST-segment depression and decremented as a function of duration of exercise and workload in watts; thallium-201 scintigraphy by means of an index for minimal to maximal perfusion region (vitality index) and redistribution factors; equilibrium-radionuclide ventriculography by means of global ejection fraction and maximum systolic volume change with respect to the end-diastolic volume. The patients were divided into three groups: 30 had successful TCA defined as demonstrating at least a 20% reduction in the stenosis; six underwent aortocoronary bypass operation (nine grafts; complete revascularization in four patients); and in six patients TCA was unsuccessful. TCA was successful in 24 LAD stenoses, 5 RCA stenoses, and in one proximal anastomosis of an aortocoronary bypass graft. Dilatation could not be achieved in three LAD stenoses and three stenoses of the RCA. In those in whom it was successful, TCA yielded an average reduction of coronary artery stenosis from 84 to 43%. Both TCA and bypass operation (OP) led to comparable degrees of functional improvement. The ischemia score decreased from 2.8 to 0.9 after TCA and from 1.6 to 0 after OP. The vitality index increased from 67 to 77% and from 74 to 81% after TCA and OP respectively while the corresponding redistribution factors decreased (TCA: at 1 hour from 5 to 1% and at 3.5 hours from 11 to 4%; OP: at 1 hour from 2.2 to 1.4% and at 3.5 hours from 7.6 to 4.1%. The global ejection fractions at rest improved from 46 to 52% and from 38 to 45% and during exercise from 42 to 50% and from 36 to 43% after TCA and OP respectively. The maximum--dV/dt/EDV increased at rest (TCA: from 2.7 to 3.5 per second; OP: from 2.1 to 3.8 per second) and during exercise (TCA: from 3.1 to 4.0 per second; OP: from 2.6 to 3.3 per second). In the group with unsuccessful TCA, no significant differences in the latter parameters were observed. Ten of the 30 patients who had undergone successful dilatation were reinvestigated after three months. Maintenance of good functional results could be documented in eight while deterioration was seen in two patients, one with a significant restenosis and one who developed a new narrowing distal to the successfully dilated stenosis. Thus, the results show that in selected cases, TCA can render improved ventricular function and perfusion comparable to that of aortocoronary artery bypass surgery.

Adult↗

[Effect of bypass surgery on the presence and quality of collaterals in coronary heart disease (author's transl)].

The presence and quality of collaterals in coronary angiograms were studied in 89 patients with CHD before and after bypass surgery as well as in 12 unoperated patients who also underwent left heart catheterization twice. Total and local evaluation of collaterals was made in terms of global and regional collateral scores as well as collateral flow rates. Total revascularization generally leads to an entire disappearance of collaterals in the angiogram and represents a criterium for assessing the success of bypass surgery. In non-revascularized as well as unoperated patients, the quality of collaterals improves. This is attributable to additional surgically induced changes in the coronary arteries and progression of the underlying disease, respectively. Partially revascularized patients display no definite changes in total collateral score. In these cases, collaterals to the revascularized regions diminish, whereas those to non-revascularized regions increase. Myocardium not revascularized directly by an aortocoronary bypass graft is thus indirectly revascularized via the secondary appearance of collaterals, which enhance regional perfusion.

Adult↗

[Left ventricular function at rest and during leg raising in patients with cardiomyopathy (author's transl)].

Isovolumetric and auxotonic contractility parameters were analyzed at rest and following leg raising in 16 patients with predominantly congestive cardiomyopathy. Regional ventricular function was calculated using the hemiaxis method. In patients with mild cardiomyopathy, ventricular function improved following leg raising with an increase in the mean velocity of circumferential fiber shortening and a decrease in endsystolic volume. By contrast, patients with moderate and severe cardiomyopathy displayed deterioration of ventricular function with increased hypokinesia, particularly in the anterior and apical region. Endsystolic volume increased; mean velocity of circumferential fiber shortening, regional wall velocity, and ejection fraction decreased. These results suggest that in the early phase regional disturbances of ventricular function may regress in response to passive leg raising. In the severe forms of cardiomyopathy, the preexisting regional or generalized hypokinesia increased markedly following leg raising, reflecting limited or absent left ventricular contractility reserve.

Adult↗

[The effect of diltiazem and nifedipine on exercise-induced ST-segment depression and heart rate in patients with coronary heart disease (author's transl)].

In 10 patients with angina pectoris and angiographically proven coronary heart disease, the effect of 60 mg of orally administered diltiazem (D) and 20 mg of nifedipine (N) on heart rate and exercise-induced ST-segment depression was investigated under randomized double-blind conditions. A significant reduction in mean ST-segment depression could be observed at 90 and 180 minutes for N (-36% and -33%) and D (-28% and -27%). One patient did not improve after D; two patients showed a paradoxic increase in ST-segment depression after N. Mean heart rate at rest, during, and after exercise compared to the drug-free periods was lower for D and higher for N. The difference in mean heart rate between N and D was significant (p less than 0.001). In respect to their ability to reduce ST-segment depression, 20 mg of N appears to be nearly equipotent to 60 mg of D. The different effects of D and N on heart rate and AV condition must be considered in certain clinical settings.

Adult↗

[Significance of collaterals in protection of resting myocardial function in coronary heart disease (author's transl)].

The significance of collaterals for left ventricular function at rest was studied on the basis of 345 consecutive angiographies of patients with coronary heart disease. According to the severity of coronary stenosis, patients were assigned to groups with one-, two-, and three-vessel disease. Subgroups were formed based on the extent of narrowing in percent. All angiograms were examined for the presence and absence of collaterals. The significance of the collaterals in evidence was quantified in terms of a collateral score. To assess left ventricular function, global (left ventricular enddiastolic pressure, left ventricular enddiastolic volume, left ventricular ejection fraction) and regional (percentage hemiaxis shortening) parameters were employed. Within the groups with the same degree of coronary stenosis, no differences in left ventricular function were observed even when regrouping was carried out according to the presence or absence of collaterals. The collateral score, however, suggested that left ventricular function was better in patients with good collaterals than in those with poor collaterals. Regional parameters of left ventricular function underscore the protective effect of collaterals for left ventricular function at rest particularly clearly. Global parameters of left ventricular function do not demonstrate this relationship quite as decisively, since regional disturbances of contractile function may be compensated for by hypercontraction of other wall areas.

Coronary Angiography↗

[Correlation between isovolumic and auxotonic indexes of left ventricular contractility at rest and during exercise (author's transl)].

The validity of isovolumic parameters of left ventricular contractility in assessing ventricular function at rest has been questioned repeatedly, and with some justification. By contrast, auxotonic parameters such as left ventricular ejection fraction provide a clinically useful index of functional impairment even under resting conditions. The correlation between isovolumic and auxotonic parameters during exercise remains unclear, however. To evaluate this relation, isovolumic m (max dP/dt, Vpm) and auxotonic (EF, Vcf) parameters of contractility were determined simultaneously at rest and after both leg raising and exercise using a manometer-equipped angiography catheter in 45 patients. Under resting conditions, there was no significant correlation between the parameters (Vpm: Vcf,r = 0,226). After leg raising (r = 0.543) and exercise (r = 0.801), the correlation became markedly closer. The presence of hypo- or akinetic regions did not affect the correlation. In patients with cardiomyopathy and uniform functional impairment, the correlation did not improve in comparison with the group of patients characterized by asynergy. The specificity of the various parameters was evaluated in patients with and without significant coronary-artery stenosis. The Vcf values during exercise yielded virtually optimal separation of the two groups, whereas isovolumic parameters were far less specific.

Blood Volume↗

[Diagnosis and treatment of chylopericardium (author's transl)].

In a 22-year-old patient without clinical symptoms, a chylous pericardial effusion was found as cause of pericardial enlargement persisting over 7 years. Ultrasonic echocardiography, diagnostic pericardial puncture and the demonstration of chylomicrons enabled the diagnosis to be made. Lymphography showed lymphangiectasis of the thoracic duct. At operation two fistulous connections between pericardium and lymphatic system were found. Surgical ligature of the thoracic duct and the lymphatic fistulae and pericardial fenestration resulted in rapid normalisation of all findings.

Adult↗

Controlled study of intravenous nitroglycerin treatment for two days in patients with recent myocardial infarction.

Hemodynamic measurements were obtained for 48 h in 46 patients with recent myocardial infarction. Patients were randomized to treatment with (n = 22) and without nitroglycerin (NTG) n = 24). In patients with diastolic pulmonary arterial pressure (PAEDP) less than 20 mmHg (group I), NTG decreased PAEDP from 15 to 11 mmHg (n = 13); in the untreated control group PAEDP remained unchanged (n = 15). Cardiac output decreased in the NTG group from 5.4 to 5.0 1/min and in the control group from 4.7 to 4.4 1/min. Mean arterial pressure decreased in both groups, in the NTG group from 106 to 97 mmHg and in the control group from 102 to 94 mmHg. In patients with left ventricular failure and PAEDP greater than 20 mmHg (group II) the decrease in left ventricular filling pressure was significantly greater (25 to 17 mmHg, n = 9) than in the control group (24 to 20 mmHg, n = 9). Cardiac output increased during NTG treatment from 4.2 to 5.1 1/min. In the control group, however, cardiac output decreased from 4.2 to 3.6 1/min. Mean arterial pressure decreased from 103 to 95 mmHg in the NTG group and from 114 to 96 mmHg in the control group. Heart rate did not change significantly. Thus, PAEDP decreased significantly in patients who received NTG treatment for 48 h compared to an untreated control group. Cardiac output increased in treated patients, especially those with left ventricular failure, but decreased in the control group. Mean arterial pressure decreased to the same degree in treated patients and in controls.

Aged↗

Comparison of antiarrhythmic effects of oral prajmalium bitartrate and intravenous lidocaine in acute myocardial infarction.

In 35 patients with acute myocardial infarction premature ventricular complexes were quantified from stored continuous electrocardiographic tape recordings using a semiautomated arrhythmia detection system. Seventeen patients, separated at random, received no antiarrhythmic drug and formed the control group. In nine patients prajmalium bitartrate was given orally at a dose of 60 mg. (20 mg. every 4 hours). Nine patients had permanent infusions of 2.1 mg./minute lidocaine (corresponding to a daily dose of 3 g.). In both treated groups premature ventricular complexes decreased significantly as compared to the spontaneous frequency in the control group. Six hours after the onset of therapy premature ventricular complexes were reduced to 37% of the initial value in the prajmalium bitartrate group and to 51% in the lidocaine group, whereas in the control group frequency increased (169%). The peak effect was reached after ten hours when premature ventricular complexes were reduced to 5% under prajmalium bitartrate and to 20% under lidocaine administration. Runs of premature ventricular complexes were nearly completely suppressed after administration of prajmalium bitartrate. Under lidocaine administration runs were moderately and not significantly reduced. Eight hours after the onset of therapy, runs were reduced to 8% of the initial value under prajmalium bitartrate and to only 79% under lidocaine. The effect of prajmalium bitartrate on runs of premature ventricular complexes was significantly more pronounced than the effect of lidocaine. The present study documents that orally administered prajmalium bitartrate is an alternative to intravenous administration of lidocaine in the treatment of ventricular arrhythmias after acute myocardial infarction.

Administration, Oral↗

[Reduction of CK and CK-MB enzyme levels as indicators of infarct size by intravenous nitroglycerin (author's transl)].

Intravenous nitroglycerin has beneficial effects on hemodynamics and on myocardial ischemia. The aim of the present study was to investigate whether it also reduces final infarct size. In 60 patients with myocardial infarction serial blood samples were tested for creatine kinase (CK) and its isoenzyme CK-MB activity for infarct size calculations. Hemodynamic parameters were measured every 4 hours. Patients were randomized to a control (n = 29) and a nitroglycerin group (n = 31). In the early intervention group continuous perfusion of nitroglycerin for 48 hours was started < 8 hours (mean 4.5 hours) after onset of symptoms, and in the late intervention group > 8 hours (mean 12.8 hours) after onset of symptoms. In early intervention (n = 22) peak CK activity was 871 U/l in control patients and 544 U/l (p < 0.05) in the nitroglycerin group. The rate of CK release was reduced from 79 to 33 U/l x h, i.e. by a total of 58%, as was total CK and CK-MB release (p < 0.02). Calculated CK infarct size was 69 g equiv. in controls and 48 g equiv. in the nitroglycerin group. (CK-MB: 68 versus 43 g equiv., p < 0.05). In late intervention (n = 28) the differences were less pronounced. Nitroglycerin reduced left ventricular filling pressure significantly and increased cardiac output. Blood pressure changed insignificantly and peripheral vascular resistance decreased. In conclusion, nitroglycerin reduces CK and CK-MB release and hence calculated infarct size, particularly when treatment is begun within the first 8 hours after onset of symptoms.

Aged↗

[The influence of ergonovine on coronary artery diameter and hemodynamics in patients with angina pectoris at rest (author's transl)].

The influence of methyl ergonovine on coronary artery diameter and regional ventricular function was studied in three groups of patients with and without suspected coronary artery spasm. Ten patients with angina at rest in whom spasm was suspected were compared to seven coronary heart disease patients with stable effort angina. Six patients without coronary heart disease served as controls. Ergonovine, an agent known to cause coronary vasoconstriction, was administered in order to identify the possible role of spasm in the various subgroups. The standardized study procedure comprised coronary and left ventricular angiography before and after 0.1 to 0.4 mg ergonovine i.v. as well as after 1.6 mg nitroglycerin sublingually. Following ergonovine provocation, narrowing of the anterior descending branch averaged 22 per cent in the patient group with suspected spasm, 3 per cent in patients with coronary heart disease, and 6 per cent in the control group. The spasm group also displayed regional ventricular hypokinesis and an increase in endsystolic volume. LVEDP increased from 15 +/- 6 to 28 +/- 7 mm Hg (p < 0.0005) mean circumferential fiber shortening (mean Vcf) decreased from 1.6 +/- 0.4 to 1.1 +/- 0.4 circ/s (p < 0.0025), and the velocity of shortening in the anterior apical hemiaxis (Vm3) declined from 1.9 +/- 0.2 to 0.8 +/- 0.4/s (p < 0.0005). These changes were much less evident in the coronary heart disease group. No significant hemodynamic changes were observed in the control group. Patients with angina at rest are much more susceptible to ergonovine-induced coronary artery narrowing than patients with stable exertional angina.

Adult↗

[Frequency, localization and severity of coronary artery stenoses in correlation to age (author's transl)].

Angiograms of three different groups of patients were examined as to incidence, localization and severity of regional and overall coronary stenoses in correlation to age (group I = 217 patients with valvular and congenital heart disease, 174 patients with coronary heart disease without [group II] and after infarction [group III = 251 patients]). In group I the incidence and number of stenoses increased significantly with age, but not the severity of stenoses. In group III the age dependency of the number of stenoses was less significant and again there was no age correlation to the severity of stenoses. In group II no correlation of the examined parameters to age was found. Judging the severity of coronary sclerosis by a special score, there was a significant increase in group II compared to I and in III compared to II. Furthermore, this coronary score correlated to age in group I and III. In all three groups the stenoses were most frequently found in the proximal parts of the vessels independent from age. Stenosing coronary sclerosis is not an age-induced disease. Its more frequent incidence in older patients is caused by the longer lasting effect of risk factors with aging. Once symptomatic with angina pectoris, the coronary anatomy, does not depend on age. Thus regarding coronary anatomy, coronary bypass grafting should be equally possible in the elderly patients as in the younger ones. In patients with myocardial infarction, the number of diseased vessels increased with age.

Adult↗