Heart attack survivors have a lower risk of contracting Parkinson’s disease

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People who have had a heart attack may be slightly less likely than people in the general population to develop Parkinson’s disease later in life, according to new research published today in the Journal of the American Heart Association, an open access, peer-reviewed journal of the American Heart Association.

Parkinson’s disease is a brain disorder characterized by progressive loss of physical movement, including tremors, slow or slurred speech, and/or stiffness or limited range of motion for walking and other physical activities. There is no cure for Parkinson’s disease, and it is also associated with behavioral changes, depression, memory loss and fatigue. Secondary parkinsonism, which has symptoms similar to Parkinson’s disease, may be caused by stroke, psychiatric or cardiovascular medications, or other illness.

“We have previously found that following a heart attack, the risk of neurovascular complications such as ischemic stroke [clot-caused stroke] or vascular dementia is markedly increased, so the finding of a lower risk of Parkinson’s disease was somewhat surprising,” said lead study author Jens Sundbøll, M.D., Ph.D., from the departments of clinical epidemiology and cardiology at the Aarhus University Hospital in Aarhus, Denmark.

“These findings indicate that the risk of Parkinson’s disease is at least not increased following a heart attack and should not be a worry for patients or a preventive focus for clinicians at follow-up.

“It is not known whether this inverse relationship with risk of Parkinson’s disease extends to people who have had a heart attack. Therefore, we examined the long-term risk of Parkinson’s disease and secondary parkinsonism among heart attack survivors,” Sundbøll said.

The researchers examined health registries from the Danish National Health Service. They compared the risk of Parkinson’s disease and secondary parkinsonism among about 182,000 patients who had a first-time heart attack between 1995 and 2016 (average age 71 years old; 62% male) and more than 909,000 controls matched for age, sex and year of heart attack diagnosis. The results were adjusted for a variety of factors known to influence the risk of either heart attack or Parkinson’s disease.

Over a maximum continual follow-up of 21 years, after adjusting for a wide range of potential confounding factors, the analysis found that, when compared to the control group:

  • there was a 20% lower risk of Parkinson’s disease among people who had a heart attack; and a 28% lower risk of secondary parkinsonism among those who had a heart attack.

“For physicians treating patients following a heart attack, these results indicate that cardiac rehabilitation should be focused on preventing ischemic stroke, vascular dementia and other cardiovascular diseases such as a new heart attack and heart failure, since the risk of Parkinson’s appears to be decreased in these patients, in comparison to the general population,” Sundbøll said.

Heart attack and Parkinson’s disease share certain risk factors, with higher risk found among elderly men and lower risk among people who drink more coffee and are more physically active. Interestingly, however, some classic risk factors for a heart attack—such as smoking, high cholesterol, high blood pressure and Type 2 diabetes—are associated with a lower risk of Parkinson’s disease.

In general, more heart attack patients smoke and have elevated cholesterol, either of which may explain the slightly reduced risk of Parkinson’s disease among heart attack survivors.

“There are very few diseases in this world in which smoking decreases risk: Parkinson’s disease is one, and ulcerative colitis is another. Smoking increases the risk of the most common diseases including cancer, cardiovascular disease and pulmonary disease and is definitely not good for your health,” Sundbøll noted.

One limitation of the study is that there was not enough information about smoking and high cholesterol levels among the participants, which may have influenced the findings. In addition, the study population was vastly of white race/ethnicity, according to Sundbøll, therefore, the findings may not be generalizable to people from diverse racial or ethnic groups.

Co-authors are Szimonetta Komjáthiné Szépligeti, M.Sc.; Péter Szentkúti, M.Sc.; Kasper Adelborg, M.D., Ph.D.; Erzsébet Horváth-Puhó, M.Sc., Ph.D.; Lars Pedersen, Ph.D.; Victor W. Henderson, M.D., M.S.; and Henrik Toft Sørensen, M.D., Ph.D., D.M.Sc.


BUT…..

Our study found that individuals with stroke were more likely to have PD, which was consistent with someReference de Laat, van Norden and Gons 7 , Reference Becker, Jick and Meier18 – Reference Patel, Coutinho and Emsley20 but not all previous studies.Reference Ghebremedhin, Rosenberger and Rub 21 , Reference Song, Kim, Cho and Chung22 Interestingly, increased risk of stroke was also found in PD in a recent community-based study.

Reference Huang, Chen and Yen 19 Cerebral small-vessel disease was shown to be associated with mild parkinsonian signs in several cohorts. Vessel lesions in certain locations were suggested, accounting for the link between stroke and PD, including frontal and parietal white matter lesion or lacunar infarcts in the thalamus.

Reference Hatate, Miwa and Matsumoto 6 – Reference Reitz, Trenkwalder, Kretzschmar, Roesler, Von Eckardstein and Berger8 Recently, small cerebral vascular changes such as microbleeds were also found to be associated with idiopathic PD.Reference Kim, Park, Kim, Ma and Kim 23 DJ-1, a gene causing familial PD, was shown to be involved in cerebral ischemia changes in in vitro and in vivo models, indicating another possible mechanism linking PD and stroke.

Reference Kitamura, Watanabe and Taguchi 24 , Reference Dongworth, Mukherjee and Hall25 However, neuropathological studies showed an inverse association of vascular lesions with PD lesions in the brains of autopsy-proven PD cases or dementia with Lewy bodies.Reference Ghebremedhin, Rosenberger and Rub 21 , Reference Schwartz, Halliday, Cordato and Kril26 Therefore, more studies will be needed to further investigate the association between stroke and PD and to reveal the underlying mechanisms.

We also found that history of CAD might be associated with an increased risk of PD, independent of traditional risk factors such as age, male sex and smoking. Our finding was consistent with Liang’s study, which showed an increased risk of acute myocardial infarction in PD (hazard ratios=1.46).Reference Liang, Huang and Pan 27 One possible explanation is that these two diseases share a common pathogenesis mechanism. Diabetes, hypertension and hypercholesterolemia were found to be associated with PD and CAD in epidemiological studies.

Reference Hu, Antikainen, Jousilahti, Kivipelto and Tuomilehto 1 – Reference Xu, Park and Huang3 , Reference Franklin, Gokhale and Chow28 It was possible that these vascular risk factors might contribute to PD and CAD through the same mechanisms. Another explanation for the relationship between CAD and PD is cardiac sympathetic denervation in PD. Cardiac sympathetic nerve is quite sensitive to ischemia.Reference Guertner, Klepzig and Maul 29 Chronic cardiac sympathetic denervation might aggravate the cardiac ischemia by sustained elevation of end-diastolic pressure after ischemia.Reference Lavallee, Amano, Vatner, Manders, Randall and Thomas 30 In PD with orthostatic hypotension, chronic hypotension might result in exaggerated response to exogenously given adrenergic receptor agonists, a phenomenon called “denervation supersensitivity”.Reference Senard, Valet and Durrieu 31 , Reference Imrich, Eldadah and Bentho32 Thus, it is possible that cardiac sympathetic denervation contributes to the risk of CAD by aggravating the damage to myocardial ischemia through abnormal pressure change after ischemia. Certainly, more studies need to be performed to confirm this assumption in the future.

Although anti-parkinsonian medications such as levodopa were found to exert cardiovascular side effects, our further analysis including only PD without levodopa or dopamine receptor agonist revealed similar results. These findings suggested that the association of PD and CAD was not mediated by medication such as levodopa or dopamine agonist. However, as the sample size of drug-naïve PD cases was extremely small, the results should be read cautiously.

Caffeine consumption and smoking were shown to be protective for PD in various epidemiological studies.Reference Ma, Liu, Neumann and Gao 33 , Reference Ascherio and Schwarzschild34 In our study, tea consumption was lower in PD groups than in controls in both cohorts, but only reached statistical significance in the Malu community. However, smoking consumption was significantly higher in PD groups than in controls in the Malu community, but not in the Wuliqiao community. The negative or even inverse findings might be attributed to the small sample size, methodological difference and so on.

The strengths of our study are a door-to-door survey avoiding referral bias and PD diagnosis by movement disorders specialists. However, there are still some limitations. First, there were only 159 confirmed PD patients (97 from Malu and 62 from Wuliqiao) found in our door-to-door study.

Estimated prevalence of PD in Shanghai elderly ≥50 years older will be 0.5% in the rural community and 1.7% in the urban community, which was quite low compared with other epidemiological studies for the rural community.Reference Zhang, Roman and Hong 35 Although we trained the local doctors to screen PD patients, there is a high possibility that they lost some PD patients, especially for rural local doctors. Second, history of stroke and CAD was obtained by self-reporting.

There might be some inaccuracy in the information provided by self-reporting history. More than 90% of CAD and stroke cases in the Wuliqiao community were diagnosed by specialists and more than 50% of CAD and stroke cases in the Malu community were diagnosed by specialists, indicating a comparable reliability of CAD and stroke diagnosis in our cohorts. However, self-recollected information of CAD might render a recall bias, as well as an understanding of the different diagnosis and educational levels, which may play an important role in our results. Third, our study was retrospective and performed in Chinese Shanghai area, and thus the results represent the population in Shanghai.

In conclusion, we found that history of stroke and CAD was associated with PD in two Chinese population-based cohorts. These findings suggest that vascular disease might play some role in the pathogenesis of PD. Therefore, it is still important to investigate the mechanism linking stroke and CAD with PD, and probably prevent or treat PD by modifying vascular factors in the future.

REFERCE LINK :https://www.cambridge.org/core/journals/canadian-journal-of-neurological-sciences/article/stroke-and-coronary-artery-disease-are-associated-with-parkinsons-disease/FD276F0FF751DED00E45C9174028F6AF


More information: Journal of the American Heart Association (2022). www.ahajournals.org/doi/10.1161/JAHA.121.022768

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