Search PubMed⌕ Search

Biomedical subjects

J Thormann

Publications and source records attributed to J Thormann.

At least 73 records · Page 4Linked to original sources
PubMed1984

[Hemodynamic significance of the coordination of atrial and ventricular systole in tachycardia].

In 15 patients, aged 55.6 +/- 3.7 years with normal LV-function, the comparison of hemodynamic results as induced by ventricular pacing (VP) (at 110, 140 and 170 bpm) versus atrio-ventricular pacing (AVP) (AV-sequences: 30, 130 and 230 msec) revealed the following: VP with increasing rates inversely proportionally compromised AO-pressure by an average of -7, - 19 and -28% respectively, and cardiac output (CO) by an average of -2, -12 and -26% respectively. However, AVP with an AV-sequence of 130 msec, at the same 3 basic rates, clearly proved hemodynamically superior in comparison, in that AO-pressure dropped significantly (by an average of -13%) only at 170 bpm, an CO even showed tendencies to increase at 110 and 140 bpm (by an average of +17 and +7% respectively), finally decreasing by a mere -11% at 170 bpm only. Pacing, when using AV-sequences of 30 and 230 msec, resulted in an impairment of AO-pressure and CO of the same range as during VP at equal rates. Thus, beneficial hemodynamic results, AVP versus VP, have been proven also for rapid-rate pacing in normal ventricles, provided the AV-sequence is optimal (130 msec for the present patient group) but not in any incoordinate range of AV-sequences (as for instance 30 and 230 msec), with which beneficial atrial transport function cannot be achieved.

Blood Pressure↗
PubMed1984

[Regularization of ventricular intervals in atrial fibrillation--electrophysiologic findings on the underlying mechanism].

In 13 patients with chronic atrial fibrillation, programmed right ventricular pacing was performed before and after intravenous administration of 4 mg gallopamil. Application of the Ca-antagonist resulted in a marked decrease in the ventricular response in all and in a regularization of the ventricular response (variation coefficient of the ventricular cycle length: less than 10%) in 7 of 13 cases, while atrial fibrillation persisted. During regularization right ventricular extrastimulus testing showed a constancy of the postextrasystolic interval irrespective of the changes in the coupling interval of the extrasystole. The postextrasystolic cycle was slightly longer than the basic cycle; the difference amounts to a mean value of 107 +/- 22 ms. During the control period the postextrasystolic cycle showed the same irregularity as the basic cycle. The same random distribution was observed if the first 10 cycles of the spontaneous rhythm were analyzed after a short period of ventricular overdrive pacing. After regularization the first 2-3 postpacing cycles were markedly prolonged, and during the following cycles a gradual adjustment to the length of the basic cycles before overdrive pacing was seen, resembling the warming up of a pacemaker. It is concluded that regularization is most probably due to atrioventricular nodal depression and the occurrence of a junctional escape pacemaker.

Adult↗
PubMed1984

Influence of fluid removal rate during hemodialysis on left ventricular performance and exercise tolerance in patients with coronary artery disease.

The effect of hemodialysis (HD) on left ventricular (LV) function and exercise tolerance were measured at rest and during exercise using gated equilibrium radionuclide ventriculography in seven patients with confirmed coronary artery disease (CAD). To separate the effects of fluid removal rate on LV function in CAD, we investigated the same patients with identical overall volume loss of 4 liters during two different treatment times (4 hr and 2 hr). HD significantly increased resting LV ejection fraction (EF) from 55.7 +/- 8% to 64.7 +/- 8% (P less than 0.01) during the 4 hr HD and from 58.1 +/- 9 to 68.1 +/- 10 (P less than 0.05) during the 2 hr HD. Indicating ischemia, EF decreased at pre- and postdialysis peak exercise without differences between both treatments. HD also resulted in an improved segmental wall motion score. Exercise duration as well as S-T segment depression and angina score improved during HD, whereas heart rate, blood pressure and double product remained unchanged. We conclude that HD improves global and regional resting LV function and exercise tolerance in patients with CAD. The degree of interdialytic hydration and not the degree of fluid removal per time affects LV performance in CAD. Since LV function is the major prognostic factor in CAD, those patients require volume restriction and/or shorter interdialytic phases.

Adult↗
PubMed1983

[Complete revascularization surgery in patients with coronary disease with severely reduced left ventricular function. Discrepancies in the evaluation of results].

Clinical data, function and compliance of left ventricle as well as regional wall motion were analysed in 17 patients with preoperatively limited left-ventricular function and signs of myocardial ischaemia after complete revascularisation surgery. Recatheterisation after 5.2 months on average after surgery showed improvement by one NYHA class, an increase of mean left-ventricular enddiastolic pressure, which was interpreted as "improved status of ischaemia", a decrease of left-ventricular compliance by 30%, of enddiastolic volume by 14% and of endsystolic volume by 20% (P less than 0.05). Loss of function occurred in 3 out of 92 bypasses. Up to the time of reporting, 22.4 months postoperatively, all patients have survived in a relatively satisfactory clinical state. All parameters of left-ventricular function as well as regional wall motion showed a tendency for improvement after surgery in the majority of patients. However, pre- and postoperative mean values were not significantly different (P greater than 0.05). Thus, despite clearcut improvement of clinical state and "ischaemia index", improvement of left-ventricular function and regional wall motion are not consistently demonstrable. The reasons of this discrepancy cannot be ascertained by this investigation. The quality of the surgical intervention and the sensitivity of parameter assessment cannot be held responsible.

Blood Pressure↗
PubMed1983

Diurnal changes and reproducibility of corrected sinus node recovery time.

Corrected sinus node recovery time (CSRT) has been found unreliable in identifying all cases of sick sinus syndrome. Since other factors than sinus node dysfunction might add to the pathologic significance of the CSRT, we assessed it in 15 patients (nine group I patients with "prolonged" CSRT max = 3,196 + 2,740 msec and six group II patients with "short" CSRT max = 367 + 79 msec) at 0800, 1100, 1400, 1700, 2000, and 2300 hours with atrial overdrive stimulation rates (AST) of 90, 110, 140, 170, and 200 bpm on three consecutive days using a loop-mounted stable atrial electrode. Only with AST greater than or equal to 140 beats per minute (bpm) did all CSRTI values prove prolonged (greater than or equal to 560 msec). CSRTI values at corresponding time intervals were reproducible with AST greater than or equal to 140 bpm (day 1 vs 2 vs 3, P greater than .05), but not at AST 90 bpm and 110 bpm (P less than .05); CSRTII results, however, varied from day to day (less than .05) due to less scatter of single results. CSRTI results increased progressively with AST 90, 110, and 140 bpm from 301 + 256 msec by 60% for each pacing rate up to 785 + 848 msec. With AST greater than or equal to 140 bpm, the pattern of CSRT changes was inconsistent; this was also reflected by the distribution of the mean maxima of CSRTI: For 0800 hours at AST 140 bpm = 822 + 937 msec; for 1100 hours at AST 200 bpm = 824 + 1446 msec; for 1400 hours at AST 140 bpm = 780 + 814 msec; for 1700 hours at AST 170 bpm = 1,099 + 1,008 msec; for 2000 hours at AST 200 bpm = 1,156 + 1,280 msec; and for 2300 hours at AST 170 bpm = 1,021 + 1,102 msec. We conclude therefore that the optimal diagnostic yield for sick sinus syndrome testing is influenced by the time of the day and the AST used for CSRT testing.

Adult↗
PubMed1983

Thrombotic complications with pacemakers.

To analyze thrombotic complications, we performed brachial phlebographies in 100 consecutive patients (group 1), about 44 months after permanent pacemakers had been installed. Thirty-nine patients showed thrombotic lesions in the veins used to pass the stimulation electrode into the right ventricle. In 10 patients the medical history and in 12 patients clinical symptoms and signs indicated an impairment of venous flow. Fifteen of the 39 patients showed complete occlusion of one venous segment; collateral vessel formation was found dependent on the site and the extent of the occlusion. In the remaining 24 patients only partial occlusion without collateralization was demonstrated. Group 2 comprised 12 patients in whom the pacing lead originally inserted via right-sided veins had been severed and the free distal end left unsecured intraluminally when the second electrode was inserted via the left-sided cephalic vein. In all these patients phlebography about 19 months later revealed thrombotic complications, while 11 presented with clinical symptoms and signs. The incidence of thrombotic complications including segmental occlusion after the application of permanent pacer leads is only one-third of patients with segmental occlusion symptoms. However, since severed leads produce severe symptomatic complications in almost all cases their removal is mandatory.

Adult↗
PubMed1983

Effects of AR-L 115 BS (Sulmazol), a new cardiotonic agent, in coronary artery disease: improved ventricular wall motion, increased pump function and abolition of pacing-induced ischemia.

AR-L 115 BS (Sulmazol) is a new noncatechol, nonglycosidic cardiotonic agent. In 17 patients with significant coronary artery disease, the influence of AR-L 115 BS on hemodynamics and regional wall motion was investigated under the following conditions: 1) control, 2) the immediate postpacing period without medication, and 3) the postpacing period under the peak influence of AR-L 115 BS, 2 mg/kg intravenously. During the postpacing phase without medication, all patients developed ischemia (angina, ST segment alterations, increase of mean left ventricular end-diastolic pressure from 13 to 30 mm Hg), left ventricular pump function diminished and overall regional wall motion showed a tendency to decrease (p greater than 0.05). However, during the postpacing period with AR-L 115 BS medication, ischemia was abolished (no angina; mean left ventricular end-diastolic pressure decreased to 13 mm Hg; hemodynamic variables returned to control levels and left ventricular pump function showed some improvement while overall regional wall motion showed tendencies to improve. A comparison of alterations of hemodynamics and regional wall motion during the postpacing phase without medication with those under the influence of AR-L 115 BS shows that overall left ventricular pump function and regional wall motion improved while angina and an increase in left ventricular end-diastolic pressure were prevented. It is concluded that AR-L 115 BS improves left ventricular pump function and regional wall motion in coronary artery disease without inducing ischemia, probably by means of a reduction in extravascular resistance.

Angina Pectoris↗
PubMed1983

[Modification of hemodynamics in tachycardiac atrial fibrillation by metoprolol and verapamil].

Hemodynamic effects of the beta-receptor-blocking agent metoprolol (100 mg orally) and the calcium antagonist verapamil (160 mg orally) were analyzed in 24 patients with atrial fibrillation of different etiology (idiopathic atrial fibrillation, 6 cases; congestive cardiomyopathy, 6 cases; mitral stenosis, 5 cases; mitral regurgitation, 6 cases). 2 h after the administration of either metoprolol or verapamil heart rate was reduced significantly both at rest and during exercise. Cardiac output during exercise was significantly diminished under metoprolol in all groups of patients, whereas no effects were noted under verapamil. Peripheral vascular resistance was significantly decreased by verapamil both at rest and during exercise. No change in total peripheral resistance was noted after metoprolol at rest, but an increase occurred during exercise. Different effects on peripheral circulation may explain the different patterns of cardiac performance observed after heart rate reduction in atrial fibrillation by a calcium antagonist and a beta-blocking agent.

Atrial Fibrillation↗
PubMed1983

Myocardial perfusion and left ventricular performance during long and short haemodialysis in patients with coronary heart disease.

In seven patients with confirmed coronary heart disease and stable blood pressure control acetate haemodialysis improved left ventricular performance and exercise tolerance. Similar positive effects were obtained by a four hour dialysis (one litre fluid removal/hour) and a two hour dialysis (two litre fluid removal/hour). In this group of patients weight gain and overhydration between dialyses appears to be the major risk for myocardial perfusion and rapid weight reduction by acetate dialysis appears adequate therapy. One practical consequence from our study is to minimise fluid overload in coronary heart disease and we try to avoid iatrogenic induction of thirst by decreasing dialysate sodium from 140 mmol/litre to 125-135 mmol/litre. As far as myocardial risk factors are concerned it appears that it is more important to focus on interdialysis weight gains than on acute dialysis therapy.

Adult↗
PubMed1982

Hemodynamic and myocardial energetic changes induced by the new cardiotonic agent, AR-L 115, in patients with coronary artery disease.

AR-L 115 has been shown to improve left ventricular (LV) pump function in patients with advanced congestive cardiomyopathy by the intravenous and oral routes. Since AR-L 115 effects on myocardial oxygen consumption (MVO2) and coronary blood flow (CSF) are unknown, the hemodynamic, myocardial metabolic, and ECG responses to AR-L 115 (2 mg/kg bolus) were monitored at 9-, 14-, and 9-minute intervals in seven patients with coronary disease, exhibiting ischemia during pacing stress only. Maximal responses occurred at the fourteenth minute after AR-L 115. There were (average) increases in cardiac index by 30%, heart rate by 19%, CSF by 39%, MVO2 by 34%, and LV dp/dt max by 27%. There were (average) decreases in peak LV systolic pressure by 13%, LV end-diastolic pressure by 42%, systemic vascular resistance by 34%, and in coronary vascular resistance by 37%. All changes were significant (p less than 0.05). Myocardial lactate extraction, stroke work index, and stroke index remained unchanged (p greater than 0.05). The modest increase in MVO2 is possibly explained by the increase in contractility being partially offset by reductions in LV preload and afterload. AR-L 115-improved LV pump function was accompanied by moderate increases in MVO2 and CSF but without evidence of myocardial ischemia.

Cardiotonic Agents↗
PubMed1982

Alterations in aortic pressure and coronary blood flow: their time sequences with induced paroxysms of ventricular tachycardia in normal and impaired myocardium.

In an attempt to define more clearly the hemodynamic effects of paroxysmal tachycardia in their time sequence not only for the normal heart, we monitored coronary sinus flow (CSF), aortic mean pressure (AOMP), and coronary vascular resistance in 42 patients. They underwent stress testing of left ventricular function by paced ventricular tachycardia (VT 170/min); 13 patients had no heart disease (controls), 10 patients left ventricular hypertrophy, and 19 patients coronary artery disease (CAD). Up to the 6th s after the sudden start of VT, CSF was maintained during a 50% decrease in AOMP, while controls and hypertrophy patients with less pressure reduction (of 33 and 42%, respectively) showed a tendency to increase CSF. From the 12th to the 26th s of VT, a slight recovery of the low AOMP values took place, while CSF remained at or slightly below baseline levels. The steady state VT was characterized by further improved pressures and a CSF slightly above baseline even in CAD. Up to the 12th s after sudden stop of VT, aortic systolic pressure showed a steep increase (by 17, 13, and 8% for the three groups, respectively), while CSF dropped temporarily and after an upswing between the 12th and 26th s reached baseline levels together with AOMP. We conclude: (1) The rapidity of coronary response and its initial lag after changes of perfusion pressure are similar for normal and impaired myocardium; slight differences exist in quantity. (2) While with VT initiation perfusion pressure drops precipitously, CSF is maintained at baseline levels or slightly below even in CAD. (3) The quality of coronary hemodynamic adaptation to tachycardiac paroxysms in the impaired myocardium warrants the presence of additional operative mechanisms other than a reduced reduction in coronary vascular reserve capacity known in CAD and left ventricular hypertrophy.

Adult↗
PubMed1982

Coronary hemodynamics in simulated paroxysms of ventricular tachycardia: role of myocardial impairment and of extravascular resistance.

In 6 patients with healthy hearts (controls), 17 with coronary artery disease (CAD) and 6 with left ventricular hypertrophy due to aortic valvular disease, aortic pressure, coronary sinus blood flow (CSF) and lactate extraction were determined before and after the sudden onset of a paced ventricular tachycardia of 170 bpm (VT 170 = simulated paroxysmal ventricular tachycardia). Comparison to parameter changes during dipyridamol vasodilation revealed reduced coronary vascular reserve for CAD and hypertrophy. While VT induced a reduction of aortic pressure (stabilized by an average of 22%, and most excessively for CAD; p less than 0.05) and CSF remained at/or slightly above control levels (by an average of 31%; p greater than 0.05) equally for all groups (p greater than 0.05), lactate production in the groups with CAD and hypertrophy indicated myocardial impairment by ischemia. Excessively greater increases of CSF during dipyridamol vasodilation (vs. VT) for all groups suggested VTs extravascular resistance increase to have limited the extent of the potential of coronary vascular decrease. With one variable being kept constant (i.e. 'clamping' the vascular component of coronary resistance at its limit by dipyridamol), tachycardia during dipyridamol (D) vasodilation (VT 170+D and VT 140+D) in the controls and in the CAD group resulted in a linear decrease of CSF, allowing quantification of impaired coronary reserve for CAD. We concluded from the observations that: (1) paroxysmal VT demands fast therapeutic action foremost in the impaired myocardium, and (2) tachycardia per se acts as limiting factor for coronary blood flow via increase in extravascular resistance (aside from a shortened diastole).

Aorta↗
PubMed1982

[Efficacy of nicorandil (SG-75), a substance with nitro-properties and long-term effects in coronary patients: improvement of LV-function and wall motility without pacing-induced myocardial ischemia].

Following trials in Japan, Nicorandil (SG-75) has been introduced as a new antianginal drug with coronary dilatory properties. The effects of 20 mg SG-75 administered sublingually were studied in 9 patients with coronary artery disease and reproducible pacing-induced myocardial ischemia (MIS) (rise in left ventricular enddiastolic pressure, changes in ST-segment, and angina). Changes in heart rate, arterial pressure and angiographic left ventricular ejection parameters, contractility, parameters derived from left ventricular function (ejection fraction, cardiac index, stroke work index) and cardiac work (left ventricular stroke work index, left ventricular work), myocardial oxygen consumption, cardiac efficiency (LVeff), and regional wall motion (RWM) were investigated for the following hemodynamic phases: 7th and 14th minute after SG-75, the immediate postpacing phase without medication (PPP), and the postpacing phase under the influence of SG-75 (PPP + SG). In the 7th and 14th minute after SG-75 and in the absence of stress, there was no variation from control values (p less than 0.05). In the 15th and 16th minute after SG-75 (serum-level control), under pacing stress equivalent to that measured in the PPP, the MIS observed in the absence of medication did not now occur. Moreover, in the PPP + SG-75 phase the following mean parameter changes were noted: ejection fraction +21%, cardiac index +37%, left ventricular stroke work index +48%, left ventricular work +52%, and LVeff +60%; RWM also improved. Prophylaxis of ischemia and improved hemodynamics under the influence of SG-75 were probably due to a decrease in preload (left ventricular enddiastolic pressure -41%) and afterload (stroke volume ratio -29%). Similar changes might have been expected after nitroglycerin, if given under equivalent conditions. Since no harmful effects, either subjective or objective, were apparent during or after application of SG-75, this seems to be a promising drug for the antianginal therapy of the future.

Aged↗
PubMed1982

[Mechanism and effects of the cardiotonic AR-L 115 BS in coronary heart disease: improved ventricular function and regional wall motility without angina pectoris].

UNLABELLED: The use of new cardiotonic drugs, such as AR-L 115 BS (ARL), in patients with coronary artery disease (CAD) might be limited by their aggravating myocardial ischemia (MIS). Accordingly, we investigated ARL's (2 mg/kg BW i.v.) hemodynamics, myocardial oxygen consumption (MVO2) and regional wall motion (RWM) in 30 patients with CAD presenting with pacing-induced MIS (angina, rise of LVEDP, lactate production). ARL improved LV-pump function in 13 group-1 patients (average increases: cardiac index by +25%; LV-work by +17%; dp/dtmax by +30%; coronary sinus flow by +39%), while there was a decrease in preload (LVEDP by -44%) and afterload (AOMP by -9%) and cardiac efficiency by -25%. Such ARL-effects required a rise of MVO2 by +41% but did not induce MIS. These beneficial results were corroborated by significant hemodynamic improvements also in 17 group-2 patients when comparing the non-medicated immediate post-pacing period (PPP) with MIS versus the ARL-medicated PPP (= PPP + ARL) without MIS, where RWM improved by an overall average of 26 +/- 11% in the phase PPP + ARL. CONCLUSION: In CAD ARL improves hemodynamics and RWM. The mechanism is pre- and afterload reduction, increase in contractility, MVO2 and CSF without MIS being induced.

Cardiotonic Agents↗
PubMed1982

[Hemodynamic consequences of suddenly abolished atrial contraction].

The effects of several modes of stimulation (right ventricular pacing during sinus rhythm, right ventricular pacing during induced atrial fibrillation, and atrioventricular (AV) sequential pacing with an AV delay of 130 msec) on blood pressure and cardiac output were investigated in 10 patients with normal left ventricular function. The stimulation rates were 110, 140, and 170/min for each stimulation mode. There were no significant differences between ventricular pacing in sinus rhythm and ventricular pacing in atrial fibrillation as regards blood pressure and cardiac output. Ventricular stimulation during atrial fibrillation resulted in a significant fall in systolic blood pressure (84%, p less than 0.05) even at a rate of 140/min, whereas in AV-sequential pacing systolic blood pressure only fell to 87% of the baseline value at a rate of 170/min. A significant decrease in cardiac output occurred at rates of 140/min ventricular pacing during atrial fibrillation and at rates of 170/min with AV-sequential pacing. The results underline the importance of active ventricular filling in tachycardia. There were no significant differences in the measured parameters when ventricular pacing with AV-dissociation was compared with ventricular pacing at identical rates during atrial fibrillation.

Atrial Fibrillation↗