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Biomedical subjects

H Grendahl

Publications and source records attributed to H Grendahl.

At least 19 recordsLinked to original sources
PubMed1988

Changes in coronary haemodynamics and myocardial metabolism at rest and during exercise after a cardiotonic drug (prenalterol) in patients with coronary artery disease.

To elucidate the myocardial metabolic and haemodynamic effects of an inotropic drug in patients with coronary artery disease (CAD) without evident congestive heart failure (CHF), the acute effects of prenalterol were studied in nine patients. Patients with documented CAD by leftsided cardioangiography and end-diastolic pressure greater than 15 mm Hg were included in the study. They were examined at rest and during supine exercise at a level just below their anginal threshold before and after prenalterol. At rest, rate pressure product (RPP) increased by 40% (P less than 0.01), cardiac index rose 20% (P less than 0.01), cardiac venous flow (CVF) increased by 18% (P less than 0.05), and myocardial oxygen consumption (MVO2) increased by 20% (P less than 0.05) after prenalterol administration. Despite a decrease in mean pulmonary capillary venous pressure (PCV) of 40% (P less than 0.01), myocardial lactate extraction fell significantly (P less than 0.01) and lactate production was observed in three of nine patients compared to before prenalterol administration. During exercise, RPP increased by 20% (P less than 0.01), cardiac index remained unchanged, CVF increased by 25% (NS) and MVO2 showed a tendency to an increase (NS) after prenalterol administration. Mean PCV pressure decreased by 30% (P less than 0.01). Myocardial lactate extraction was markedly reduced during exercise (P less than 0.01) and five of nine patients showed lactate production compared to that before prenalterol administration. Thus, despite a decrease in left ventricular filling pressure, increased myocardial oxygen demand occurred after acute administration of prenalterol. Prenalterol and probably similar inotropic drugs should be used cautiously in patients with CAD without clinical evidence of congestive heart failure.

Catheterization, Swan-Ganz↗
PubMed1987

Haemodynamics during repeated exercise tests with special reference to the 'warm-up' phenomenon in patients with angina pectoris.

The haemodynamic effect of two successive supine exercise tests 20 min apart was examined in 12 patients with angina pectoris. All the patients had coronary artery disease verified by angiography and were accepted for coronary bypass surgery. They exercised 20-40 W and all of them had angina during the first exercise test. Half the patients did not experience angina during the second of the two exercise tests ('warm-up' responders). In these patients left ventricular filling pressure (LVFP) was reduced by 40% (P less than 0.01) in the second compared to the first exercise test. The non-responders showed no significant change in LVFP. The heart rate pressure product (RPP) and thus myocardial oxygen demand were unchanged in responders and non-responders. In another 10 patients with angina and coronary artery disease, also accepted for coronary bypass surgery, atropine (1.5-2.0 mg) was given intravenously. Ten minutes after administration of atropine, these patients followed exactly the same investigation programme including two successive supine exercise tests as in the group not given atropine. In the group given atropine, four 'warm-up' responders and six non-responders showed the same pattern of response in LVFP as in the group not given atropine. In the 'warm-up' responders a smaller increase in RPP was observed during the second exercise test compared to the first. The present study indicates that cholinergic mechanisms are probably not involved in the 'warm-up' phenomenon. Due to the difference in haemodynamic response, the 'warm-up' phenomenon has to be taken into account when evaluating results from haemodynamic studies of cardiovascular drugs.

Adult↗
PubMed1985

Ambulatory 24 hour ECG in patients with a history of syncope. A retrospective follow-up study over 2 years.

174 patients referred to a general hospital for unexplained syncope were examined by ambulatory 24 hour ECG (AECG) and a follow-up by questionnaire after 2 years. The AECG demonstrated sinus rhythm in 113 patients, atrial fibrillation in 15 (in 2 of these there were occasional RR intervals of more than 3 seconds), atrioventricular (AV) block in 10, sinoatrial (SA) block in 14, tachycardia or frequent ventricular extrasystoles (VES) in 21, and no recording (technical failure) in one. Ten patients got a permanent pacemaker due to these findings, and 7 were given antiarrhythmic drug therapy. 121 patients responded to the questionnaire, 37 were dead and 16 lost to follow-up. Of the 121 responders, 36 reported multiple syncopes in the follow-up period, and another 17 one syncope. Eleven patients had received a permanent pacemaker during the follow-up period.

Adolescent↗
PubMed1979

Influence of high plasma concentrations of free-fatty acids on heart rhythm in healthy fasting men.

Ten healthy male student in regular sinus rhythm fasted for 66 hours. Their overnight fasting plasma concentration of free fatty acids (FFA) was 455 +/- 104 micro mol/1 (mean +/- S.E.M., n=7), the reference value of our laboratory, measured in another normal population of young men, being 344 +/- 28 micro mol/1 (n=10). After 42 and 66 hours of fasting, the plasma concentration of FFA rose to 1198 +/- 181 (p less than 0.01, n=10) and 1471 +/- 89 micro mol/1 (p less than 0.001, n=10), respectively. During the last 24 hours of fasting, the heart rate rhythm was monitored continuously by means of a Holter recorder and computer. No arrhythmias were observed, indicating that elevated plasma concentrations of FFA, exceeding those reported in patients with acute myocardial infarction, are well tolerated by the healthy human myocardium.

Adult↗
PubMed1979

Escape rhythm in complete A-V block. The recovery phase after overdrive suppression from artificial ventricular suppression from artificial ventricular pacing.

In 60 patients with third degree A-V block, recovery of escape rhythm from overdrive suppression after ventricular pacing has been studied. Implanted unipolar VVI pacemakers were inhibited by chest wall stimuli. A total of 165 rhythmograms were studied. In 37, the rate was irregular, in the other 128 the escape rate increased gradually, following an exponential curve until stabilization after 3 minutes. In 29 of these rhythmograms, a possible exit block of the first escape impulse was observed. In 99 rhythmograms without exit block, escape rhythm recovery time was an average 1.45 times basal escape RR intervals. Overdrive suppression was most marked in patients with a slow escape rhythm.

Cardiac Pacing, Artificial↗
PubMed1978

Overdrive suppression of implanted pacemakers in patients with AV block.

Patients being permanently paced for symptomatic AV block were studied by overdrive suppression of the QRS-inhibited pacemaker, in order to observe the underlying heart rhythm. The chest wall stimulation method was used. In complete AV block the escape rhythm recovery time proved highly reproducible on repeated testing on the same day, and in many patients remained so over months or years. Occasionally, a doubling of the escape rhythm recovery time was seen, suggesting initial exit block of the escape focus. Resetting of the escape rhythm usually followed an exponential curve until stabilisation after about 3 minutes. An early escape rhythm with a recovery time of less than 4 seconds was found on every occasion in 21 of 58 patients with complete AV block, and inconstantly in 23 more; in 14 it was never observed. Accidental pacing failure was seen in 15 patients. The overdrive suppression test was helpful in selecting pacemaker dependent patients.

Aged↗
PubMed1976

Pacemaker wires and electrodes. A follow-up study.

In 362 patients on permanent pacing, a follow up with regard to pacemaker electrode function time and connection to pulse-generators has been carried out. In 12 patients Elema epicardial electrode were used with an average function time of 3.8 years. 232 Elema EMT 588 endocardial electrodes were used in 216 patients. Average observation time for the electrodes was 3.3 years. Sixty-eight electrodes have been followed for more than 5 years. Early electrode complications comprise 10 per cent of displacements before implantation of the pulse-generator and another 6 per cent of electrode displacements within the first 3 months after implantation. Eleven per cent of the electrodes had to be corrected due to high threshold value before implantation and another 6 per cent during the first 3 months after implanattion of pulse-generator. On hundred and fifty-five unipolar electrodes of the types Cordis, Medtronic, Elema EMT 282, and Stanium were implanted in 149 patients. Average observation time for the electrodes were 1.2 years. During the first 3 months after pacemaker implant 7 per cent of the electrodes were dislocated, 5 per cent failed due to high threshold value. Three perforations of the right ventricle occurred, without serious complications. Late complications i.e. after 3 months, for EMT 588 electrode included 4 per cent electrode dislocations, 4.5 per cent failure due to high threshold, 3 cases of wire break and 4 defects in the insulation. Many of the late electrode complications were probably caused by replacement operations for pulse-generators. The most frequent late complications for the conventional unipolar electrode was wire break which occurred in 5 cases.

Arrhythmias, Cardiac↗
PubMed1976

Routine pacemaker control, and selective replacement of pulse generators. A cost/benefit analysis.

Two hundred and fifty patients with permanent pacemaker have been followed up with routine pacemaker controls in a pacemaker clinic for a 21 months period 1/3-73 to 1/1-75. Ninety-five pulsegenerators were replaced. Sixty-two of the replacements were due to impending battery exhaustion, nine elective and 24 for other reasons. Signs discovered by the patients led to replacements in 21 cases for impending battery exhaustion and in 17 cases for other reasons. Forty-one replacements for impending battery exhaustion and 7 other replacements followed a scheduled visit to the pacemaker clinic. The selective replacement policy resulted in an average gain of pulsegenerator lifetime of 6.5 months, compared to a 24 minths elective replacement policy. Increased safety is obtained by routine control of pacemaker patients in a pacemaker clinic.

Action Potentials↗
PubMed1976

Diazepam in acute myocardial infarction. Clinical effects and effects on catecholamines, free fatty acids, and cortisol.

Diazepam is a valuable drug in cases of acute myocardial infarction. The 10 mg intravenous loading dose and the subsequent 15 mg oral dose of diazepam administered three times daily produced safe, pleasant sedation, and reduced the need for analgesics. A much reduced excretion of catecholamines was recorded. It is presumed that diazepam causes a lower stress reaction, which is beneficial in diminishing the incidence of malignant arrhythmias and preventing the existing myocardial injury from spreading.

Adult↗
PubMed1975

Registration of sinus node recovery time in patients with sinus rhythm and in patients with dysrhythmias.

Sinus node recovery time (SRT) after rapid atrial pacing has been recorded in 66 patients, 28 with coronary heart disease, 11 with advanced AV block, 10 with sick sinus syndrome and 17 with paroxysmal tachyarrhythmias. In patients with a normal functioning sinus node SRT was related to the basal heart rate. On an average SRT was 130% of the basal P-P interval with an upper limit of 160%. In patients with a presumed normal atrial function the mean SRT was found to be 1 080 msec, with an upper limit of 1 500 msec. This corresponds with previously published observations. In all 5 patients examined, beta-receptor blockade (propranolol 5 mg i.v.) prolonged SRT. The prolonged SRT was related to sinus bradycardia. Verapamil (Isoptin 5 mg i.v.) had no effect on SRT in the 7 patients examined. The observation of an SRT of more than 1 500 msec indicates a poor sinus node function. Recording of a normal SRT, however, cannot exclude a sinus node dysfunction, as normal SRT is occasionally found even in patients with a clinically proved dysfunction.

Arrhythmia, Sinus↗