Hypotensive Effect of Long-Term Levodopa in Patients with Parkinson’s Disease

Iwasaki, Shinichi; Hamaguchi, Katsuhiko; Iwasaki, Akira; Takakusagi, Mamoru; Narabayashi, Yohsuke

doi:10.1159/000117344

Cited by 17 publications

(11 citation statements)

References 20 publications

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“…In several other reports acute administration of levodopa has not been shown to affect cardiovascular reflexes [15,25,41,42,46] whereas some have shown that levodopa produces mild OH [5,15,32] and lowers the resting BP [5,21]. Our data indicate that although the BP level at rest was lower during levodopa treatment, levodopa does not suppress the autonomic cardiovascular responses and the sympathetic BP response to tilting.…”

Section: Discussioncontrasting

confidence: 60%

Levodopa, bromocriptine and selegiline modify cardiovascular responses in Parkinson's disease

Haapaniemi

Kallio

Korpelainen

et al. 2000

Journal of Neurology

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Autonomic nervous system (ANS) involvement is frequently found in Parkinson's disease (PD), but its causal relationship to the disease itself and its medication is unclear. We evaluated the effects of PD medications on cardiovascular ANS functions. Heart rate (HR) responses to normal and deep breathing, the Valsalva manoeuvre and tilting, and blood pressure (BP) responses to tilting and isometric work were measured prospectively in 60 untreated PD patients randomised to receive either levodopa (n = 20), bromocriptine (n = 20) or selegiline (n = 20) as their initial treatment. The results were compared with those of 28 healthy controls. The responses were recorded at baseline, after 6 months on medication and following a 6-week washout period. At baseline HR responses to normal breathing, deep breathing and tilting were already lower and the fall in the systolic BP immediately and at 5 min after tilting was more pronounced in the PD patients than in the controls. Six months' levodopa treatment diminished the systolic BP fall after tilting when compared to baseline, whereas bromocriptine and selegiline increased the fall in systolic BP after tilting and selegiline diminished the BP responses to isometric work. The BP responses returned to the baseline values during the washout period. The drugs induced no change in the HR responses. Thus PD itself causes autonomic dysfunction leading to abnormalities in HR and BP regulation and the PD medications seem to modify ANS responses further. Bromocriptine and selegiline, in contrast to levodopa, increase the orthostatic BP fall and suppress the BP response to isometric exercise reflecting mainly impairment of the sympathetic regulation.

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Section: Discussioncontrasting

confidence: 60%

Levodopa, bromocriptine and selegiline modify cardiovascular responses in Parkinson's disease

Haapaniemi

Kallio

Korpelainen

et al. 2000

Journal of Neurology

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“…Evidence exists that levodopa lowers blood pressure in hypertensive patients44 and of Parkinson's disease cases on long term treatment. 45 In addition, even parkinsonian cases not on treatment seem to have lower blood pressure than controls.39 Several observational and interventional studies have noted an increased risk of cardiovascular deaths with low blood pressure, although this still remains an issue of controversy.46 This excess risk is usually small and less than the risk we have found. Levodopa may also induce cardiac arrhythmias via its catecholaminergic actions.…”

Section: Cause Of Deathmentioning

confidence: 79%

Survival and cause of death in a cohort of patients with parkinsonism: possible clues to aetiology?

Ben‐Shlomo

Marmot

1995

Journal of Neurology, Neurosurgery & Psychiatry

194

140

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Most previous studies that have exam-ined the survival of patients with parkinsonism have recruited them from specialist centres. No previous study has ever reported cause specific mortality. We report on the mortality of a cohort of 220 parkinsonian patients recruited between 1970 and 1972 from 40 primary health care practices all over England and Wales and matched to 421 controls. At 20 years of follow up, 195 cases (88-6%) and 295 controls (70.1%) were no longer alive (P < 0.001). The median age at death for cases was 77-6 (range 53-8-97-3) and 83'5 (range 55.0-100.1) for controls (P < 0.001). The all cause hazard ratio for cases compared with controls was 2-6 (95% confidence interval (95% CI) 2.2-3.2) controlling for age, sex, and geographical region. There was little difference between men and women. Differences for cause specific mortality also emerged. Both ischaemic heart disease (2.3, 95% CI 1.5-3.4) and cerebrovascular disease (3'6, 95% CI 2.2-6.1) showed significantly increased hazard ratios. Possible reasons for these findings are discussed in terms of (a) competing causes of death, (b) a secondary effect of drug treatment, and (c) common aetiological factors for both parkinsonism and cardiovascular disease. (7 Neurol Neurosurg Psychiatry 1995;58:293-299) Keywords: Parkinson's disease; aetiology controls and may have underestimated the relative mortality as such controls are more likely to have other serious diseases. Almost all of these studies have recruited their cases from specialist neurology units. This is problematic as specialist units may, in general, recruit more atypical and severe cases of neurological diseases.'7 Only one study has been based on the follow up of a representative population based sample.'6 This study importantly reported that parkinsonian cases had a 2*5-fold greater relative risk of dying than the general population, similar and only slightly improved on the relative mortality seen for the prelevodopa era.4 This result was based on follow up for only a 3-5 year period.Cause of death among parkinsonian patients may provide a useful insight into aetiology. If they are also more likely to die of another disease, there may be a common genetic or environmental link between these disorders. No previous study has ever examined cause specific mortality of Parkinsonian cases compared with the general population.We have examined both total and cause specific mortalities of a cohort of parkinsonian cases and matched population based controls recruited from primary health care facilities followed up for a 20 year period. This avoids previous methodological problems concerning ascertainment bias and the choice of an appropriate comparative group. Our aims were (a) to determine whether the mortality of parkinsonian cases had improved since the introduction of levodopa; (b) to determine whether any possible clue to the aetiology of parkinsonism might be found if these cases were more or less likely to die of other diseases.

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“…27,28 Additionally, L-dopa and other treatments may result in resting hypotension, increased orthostatic hypotension, and increased autonomic dysfunction independent of disease severity. 22,27,[29][30][31] However, the trend of decreasing SBP after PD diagnosis was attenuated after exclusion of those on antihypertensive medications, and may thus reflect in part a stronger response to treatment of SBP in individuals with PD. Additionally, this trend after diagnosis may contribute to explain the decreased prevalence of measured hypertension in studies among diagnosed PD cases.…”

Section: Resultsmentioning

confidence: 99%