J Partanen

Helsinki University Central Hospital, Helsinki, Southern Finland Province, Finland

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Publications (24)187.85 Total impact

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    ABSTRACT: Alcohol consumption may have advantageous epidemiologic effects but ethanol also increases the risk of sudden coronary death. Prolongation of QT interval has been reported in chronic alcoholics. Long QT period predisposes to serious arrhythmias, and therefore we studied whether acute alcohol intoxication prolongs repolarization in patients with stable coronary artery disease (CAD). The effects of acute ethanol steady-state intravenous infusion (0.72 g/kg body weight within 60 min) on QT interval and QT dispersion, assessed by 12-lead electrocardiograms (ECG), were studied in 22 men with stable CAD and in 10 controls. Heart rate variability was measured by Holter recordings. Mean blood alcohol rose to 26.1 +/- 4.3 mmol/l(1.2 +/- 0.2/1000), and was maintained for 2 h. Heart rate was 56 +/- 7 beats/min before and 54 +/- 8 beats/min during ethanol infusion (NS). The heart rate-adjusted QT interval increased on the average 13-23 ms over the 12-lead ECG (p < 0.005). The QT dispersion remained unaltered. The was no difference in the repolarization response in the patients with CAD compared with the controls. The high- and low-frequency components of heart rate variability remained unaltered. In middle aged men, regardless of the presence of CAD, moderate amounts of alcohol cause prolongation of ventricular repolarization. Changes in the activity of the autonomic nervous system do not seem to explain the observed phenomenon.
    Preview · Article · Sep 1999 · Clinical Cardiology
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    ABSTRACT: Inhaled beta-2 agonists raise heart rate, systolic blood pressure and contractility, all of which cause an increase in oxygen consumption of the heart. We performed a study on the influence of inhaled salbutamol on myocardial ischaemia, rhythm, and heart rate variability as assessed by Holter monitoring of 24 patients with coronary artery disease (CAD) and clinically stable asthma or chronic obstructive pulmonary disease (COPD). In hospital the patients received 0.2 mg (hour 1), 0.4 mg (hour 6), 0.8 mg (hour 13) of salbutamol with a metered-dose inhaler and a spacer, and 5 mg (hour 25) with a nebulizer; symptoms, peak expiratory flow (PEF), 30-h Holter monitoring, and blood pressure (BP) were recorded. The study parameters were compared for the hour preceding and following each dose of salbutamol. No cardiac symptoms were associated with salbutamol inhalation. PEF increased after all doses (P < 0.005). A dose of 0.2 mg salbutamol induced no changes in heart rate, whereas dose of 0.4 mg increased heart rate from a mean of 75 +/- 13 to 79 +/- 14 beats min-1 (P < 0.005), and a dose of 0.8 mg from 76 +/- 14 to 78 +/- 15 beats min-1 (P < 0.05). No changes in systolic BP appeared after any dose of salbutamol. The diastolic BP was lowered after 0.8 mg of salbutamol from 86 +/- 12 to 82 +/- 10 mmHg (P < 0.05). The 5 mg of nebulized drug provoked no significant changes in heart rate or BP. Myocardial ischaemia, heart rate variability and ventricular arrhythmias remained unaltered with all doses. The commonly used doses of inhaled or nebulized salbutamol induced no acute myocardial ischaemia, arrhythmias or changes in heart rate variability in patients with CAD and clinically stable asthma or COPD.
    Preview · Article · May 1998 · Journal of Internal Medicine
  • J Rossinen · J Partanen · M S Nieminen
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    ABSTRACT: In order to assess additional anti-ischaemic effects of amlodipine (AML) on coronary artery disease (CAD) treated with beta-blockers, 32 patients with CAD, verified on angiograms, and stable angina were randomized to receive 5 mg/day of AML or placebo, increasing to 10 mg/day after 2 weeks. Baseline recording of 24-h ambulatory ECG and blood pressure, echocardiography and bicycle exercise test was repeated after treatment for 2 weeks and for 6 weeks. Reduction of ambulatory ischaemia was not significantly greater with AML than with placebo. In exercise tests the time to 0.1 mV ST segment depression and the total exercise time remained unaltered. Blood pressure was reduced by 10 mg AML. The total variability and the very low frequency component of heart rate were reduced after both doses. The clinical significance of the possible unfavourable change in autonomic modulation of the heart in CAD patients is not known.
    No preview · Article · Jan 1998 · Scandinavian Cardiovascular Journal
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    ABSTRACT: The effects of acute alcohol intake (ethanol blood concentration 1.3 +/- 0.4%) on heart rate variability were evaluated with 24-hour Holter recordings in 20 patients with stable coronary artery disease in a juice-controlled experiment. In the frequency domain analysis, the high-, low-, and very low frequency components were significantly decreased after alcohol: these changes last longer than the elimination of alcohol.
    No preview · Article · Mar 1997 · The American Journal of Cardiology
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    ABSTRACT: To evaluate the effect of acute alcohol ingestion on myocardial ischaemia in patients with coronary heart disease and stable angina. Randomised crossover study using fruit juice with and without ethanol. Division of cardiology in a university hospital. 20 patients with stable exertional angina and > or = 50% luminal diameter narrowing of at least one major coronary artery. Each patient was studied on two separate days, once after administration of 1.25 g of ethanol per kilogram of body weight diluted to 15% in juice, and once after an equivalent volume of juice; both tests were in the evening and lasted 90 minutes. The patients were scheduled to have 8 periods of walking for 10 min according to a time table. An ambulatory electrocardiogram and the occurrence of anginal attacks were recorded and blood pressure and blood ethanol concentration were measured until the next morning. The blood ethanol concentration (mean (SD)) rose to 28.8 mmol/l (1.3 (0.4)/1000). Alcohol raised the systolic blood pressure from 132 (16) to 141 (14) mm Hg (P < 0.05 compared with juice). The mean heart rate increased from 57 (7) to 64 (8) beats/min (P < 0.05) for 13 hours after ethanol ingestion compared with juice. The total duration of ischaemia during the ethanol test was 3.5 (median, range 0-80) min, compared with 0 (range 0-67) min for the juice test (P < 0.05). The difference resulted mainly from more silent ischaemia after ethanol ingestion (2.3 (0-80) v 0 (0-67) min; P < 0.05). The ST segment depression time integral increased during the ethanol test (4.4 (0-170) mm x min) relative to that during the juice test (0 (0-103) mm x min; P < 0.01) and especially during the following 13 hours after alcohol (3.5 (0-123) mm x min) compared with juice (0 (0-67) mm x min; P < 0.005). There were no changes in the number, duration, or ST segment depression time integral of the episodes of symptomatic angina, indicating that ethanol augmented the appearance of silent ischaemia. Acute heavy ethanol drinking aggravates myocardial ischaemia in patients with stable angina pectoris.
    Full-text · Article · Jul 1996 · Heart (British Cardiac Society)
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    ABSTRACT: Profuse spontaneous haemorrhage occurred in association with mediastinitis after median sternotomy for coronary bypass surgery in three men aged 54, 47 and 59 years. The bleeding sites were aorta, right ventricle and saphenous bypass graft. The aortic rupture occurred during closed lavage, the right ventricle ruptured during open saline mediastinal packing and the saphenous vein graft was eroded by a mediastinal drainage tube after discontinuation of closed lavage. This third patient survived and recovered, but the two others died. Previously published reports of 56 patients with 65 bleedings from this rare complication are reviewed. The outcome was fatal in 34% of cases.
    No preview · Article · Feb 1996 · Scandinavian journal of thoracic and cardiovascular surgery
  • J Partanen · M S Nieminen

    No preview · Article · May 1995 · Archives of Internal Medicine
  • Juhani Partanen · Markku Kupari · Jaakko Eränen · Juhani Kouri
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    ABSTRACT: We report intermittent mitral valve regurgitation with 17 acute pulmonary edemas over a 16-month period after aortic valve replacement due to combined aortic valve disease in a 51-year-old man. The mechanism of mitral regurgitation was explained by the relatively large size of the prosthetic valve which had had to be sutured partly below the aortic annulus. It was suspected to interfere with the closure of the mildly diseased mitral valve when under pressure or subjected to volume loadings of the left ventricle which provoked free mitral regurgitation. There was no recurrence of pulmonary edema in the 50 months following mitral valve replacement.
    No preview · Article · May 1995 · International Journal of Cardiology
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    ABSTRACT: We describe a 47-year-old man who had rapidly progressive heart failure caused by giant cell myocarditis with no response to steroid therapy. A successful heart transplantation was performed after life-threatening arrhythmias. The diagnosis was made by endomyocardial biopsy before transplantation, and it was confirmed by the histologic condition of the recipient heart. The patient has been on a triple-immunosuppression therapy with no signs of rejection or recurrence of giant cell myocarditis 23 months after surgery.
    No preview · Article · Jan 1994 · The Journal of Heart and Lung Transplantation
  • J Partanen · M S Nieminen · K Luomanmäki

    No preview · Article · Oct 1993 · New England Journal of Medicine
  • J Partanen · M Kupari

    No preview · Article · Feb 1993 · Duodecim; lääketieteellinen aikakauskirja
  • M S Nieminen · J Partanen
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    ABSTRACT: Although beta-blockers have held their own as the cornerstones of cardiological treatment for almost twenty years, the beneficial effects of these classic agents are not always appreciated in clinical work. Simplified hypertensive treatment or other factors may sometimes argue for the use of newer medicines, but many pathophysiological manifestations of high blood pressure are still best controlled with beta-blockers. The range of available preparations has increased and new compounds are continually appearing on the market.
    No preview · Article · Feb 1992 · Nordisk medicin
  • J Partanen · M S Nieminen

    No preview · Article · Jan 1992 · JAMA The Journal of the American Medical Association
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    ABSTRACT: The vascular element of a mixed type of rejection after orthotopic heart transplantation did not respond to steroid therapy in a 30-year-old man. Plasmapheresis was associated with the resolution of the clinical signs of rejection and the microscopic changes of vasculitis in the biopsy specimen. This case suggests that plasmapheresis may be useful in the treatment of acute vascular rejection in heart transplantation.
    No preview · Article · Jan 1992 · The Journal of Heart and Lung Transplantation
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    J Partanen · M Kupari · J Heikkilä · P Keto
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    ABSTRACT: A 47-year-old man with apical hypertrophic cardiomyopathy and an apical left ventricular aneurysm with palpitation as the initial manifestation is described. There was no intraventricular pressure gradient. The aneurysm is suggested to be a part of the myocardial disease or to be caused by myocardial bridging of the left anterior descending coronary artery demonstrated by angiography. The 24-hour ambulatory ECG recording showed only isolated ventricular ectopic beats and the clinical course has been favorable during 20 months without therapy.
    Full-text · Article · Nov 1991 · Clinical Cardiology
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    ABSTRACT: Cytomegalovirus infections are common disorders after heart transplantations. Manifestation of the virus without a clinical disease is still more prevalent. Differentiation of clinical infections from cytomegalovirus activations without major pathogenetic importance issues a challenge in the follow-up of patients with cardiac transplants. The case describes a 56-year-old female patient with a multiple organ lethal infection and myocarditis due to cytomegalovirus diagnosed during life with endomyocardial biopsy.
    Full-text · Article · Oct 1991 · Clinical Cardiology
  • J Partanen · T J Pellinen

    No preview · Article · Feb 1989 · Archives of Internal Medicine
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    J Partanen · J Heikkilä · T Pellinen · M S Nieminen
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    ABSTRACT: 1. Eight healthy subjects were studied before digoxin and after successive therapy periods of 1 week 0.125, 0.25 and 0.50 mg of digoxin. The mean serum concentrations (± s.d.) were 0.4 ± 0.2, 0.6 ± 0.3 and 1.4 ± 0.5 nmol l-1, respectively. The effects of digitalis were studied by echocardiography and systolic time interals at rest and after 3 min handgrip exercise. Effects of simultaneous autonomic blockade induced by atropine and propranolol were also examined. 2. Digoxin in increasing doses slowed the heart rate at rest; with the daily dose of 0.50 mg from 63 ± 10 to 53 ± 6 beats min-1, and fractional shortening rose from 28 ± 6 to 33 ± 3% (P < 0.05 for both). Preload, afterload and cardiac output did not change. The electromechanic systolic time index (QS2I) decreased (P < 0.001) and the observed alteration of QS2I was dose-related. 3. The influence of digoxin was similar during isometric exercise, except for unchanged fractional shortening. 4. During autonomic blockade digoxin slowed the intrinsic heart rate from 93 ± 6 to 86 ± 6 beats min-1 (0.25 mg) and to 83 ± 6 beats min-1 (0.50 mg) (P < 0.01 for both). QS2I was shortened (P < 0.01). Echocardiographically determined ejection phase indices remained unchanged. 5. When handgrip stress was induced during autonomic blockade, digoxin evoked a clear-cut increase in contractile function, resembling the effects of digoxin alone at rest. Thus, functional shortening increased by 14% and QS2I decreased by 16 ms (P < 0.01 for both). 6. We conclude that digoxin increases the contractility in normal heart without changes in loading conditions. The rise in inotropy at rest is obvious from both fractional shortening by echo and systolic time intervals. The same takes place during handgrip with autonomic blockade, when the heart lacks sympathetic support. The influence of long-term digoxin on heart rate is partly direct without autonomic mediation. The effect of digoxin is dose-dependent.
    Preview · Article · Apr 1988 · British Journal of Clinical Pharmacology
  • Erkki Haapanen · Juhani Partanen · Timo J. Pellinen
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    ABSTRACT: The etiology and clinical course of acute nontraumatic rhabdomyolysis and ensuing renal failure was surveyed in a series of 40 consecutive patients. In 28 cases the muscle damage occurred after excessive consumption of ethyl alcohol and/or other intoxications. Prolonged lying immobilized was the reason or contributing factor for rhabdomyolysis in 22 cases. The other evident etiologies were convulsions, vigorous physical exercise, arterial occlusion and hypothermia. Typical local signs of rhabdomyolysis--pain, swelling and weakness of the affected muscles--were absent in one fourth of the patients. In these cases the diagnosis was based on transient elevation of serum creatine kinase enzyme activity. Dialyses were required to manage acute renal failure in 24 subjects. All 36 survivors recovered normal renal function. Neurological defects in the extremities still persisted in 16 patients at three months' follow-up.
    No preview · Article · Feb 1988 · Scandinavian Journal of Urology and Nephrology
  • J Partanen · T Pellinen · M S Nieminen
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    ABSTRACT: Sixteen healthy young volunteers were studied with echocardiography and systolic time intervals at rest and after three minutes' isometric exercise before and during autonomic blockade with atropine and propranolol. Isometric exercise increased cardiac output by raising the heart rate from 64 +/- 3 to 72 +/- 4 bpm (SEM) (p less than 0.01). Mean blood pressure increased from 86 +/- 2 to 104 +/- 3 mmHg (p less than 0.001) without any changes in the calculated total peripheral vascular resistance. Afterload (left ventricular systolic wall stress) rose but preload (left ventricular end-diastolic diameter, LVEDD) did not change. There was no variation in fractional shortening, maximal velocity of circumfertial fibre shortening (VCFmax) or pre-ejection period (PEP) despite increased afterload. This indicates stimulated intropy during isometric exercise. Autonomic blockade enhanced cardiac output by increasing heart rate from 64 +/- 3 to 97 +/- 2 bpm (p less than 0.001). Mean blood pressure rose from 86 +/- 2 to 93 +/- 2 mmHg (p less than 0.01) while vascular resistance fell. Afterload did not change but LVEDD shortened form 45.5 +/- 0.9 to 43.5 +/- 0.9 mm (p less than 0.001). Preload-independent VCFmax did not increase despite raised heart rate. PEP rose from 99 +/- 4 to 107 +/- 3 ms (p less than 0.01) and fractional shortening fell from 29 +/- 1 to 25 +/- 1% (p less than 0.001); these changes were greater than expected from the reduced preload. Consequently autonomic blockade seems to impair myocardial contractility despite vagal dominance at rest. Heart rate and cardiac output were not influenced by isometric exercise during autonomic blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
    No preview · Article · Feb 1988 · Annals of clinical research