Increased prevalence of silent myocardial ischaemia and severe ventricular arrhythmias in untreated patients with Alzheimer's disease and mild cognitive impairment without overt coronary artery disease

2008 ◽  
Vol 110 (8) ◽  
pp. 791-796 ◽  
Author(s):  
Roberto Zulli ◽  
Franco Nicosia ◽  
Barbara Borroni ◽  
Chiara Agosti ◽  
Paola Prometti ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Coronary Artery Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Coronary Artery ◽  
Myocardial Ischaemia ◽  
Ventricular Arrhythmias ◽  
Silent Myocardial Ischaemia ◽  
Artery Disease

Incidence of ventricular arrhythmias during silent myocardial ischaemia in coronary artery disease

1996 ◽  
Vol 57 (1) ◽  
pp. 61-67 ◽  
Author(s):  
F. Parthenakis ◽  
G. Kochiadakis ◽  
E. Simantirakis ◽  
E. Zuridakis ◽  
S. Chrysostomakis ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Myocardial Ischaemia ◽  
Ventricular Arrhythmias ◽  
Silent Myocardial Ischaemia ◽  
Artery Disease

scholarly journals C-338A Polymorphism of the Endothelin-Converting Enzyme (ECE-1) Gene and the Susceptibility to Sporadic Late-Onset Alzheimer’s Disease and Coronary Artery Disease

2008 ◽  
Vol 24 (3) ◽  
pp. 175-179 ◽  
Author(s):  
Renato Scacchi ◽  
Giuseppe Gambina ◽  
Elisabetta Broggio ◽  
Maria Ruggeri ◽  
Rosa Maria Corbo
Keyword(s):  
Alzheimer’S Disease ◽  
Coronary Artery Disease ◽  
Alzheimer's Disease ◽  
Coronary Artery ◽  
Late Onset ◽  
Protective Role ◽  
Converting Enzyme ◽  
Significant Difference ◽  
Endothelin Converting Enzyme ◽  
Artery Disease

The human endothelin-converting enzyme (ECE) is involved inβ-amyloid synthesis and regulation of the endothelin-1 (ET-1) vasoconstricting peptide. We investigated the distribution of the C-338A polymorphism of the ECE-1b gene in sporadic late-onset Alzheimer’s disease (LOAD) and in coronary artery disease (CAD) to verify its role in the onset of these two complex diseases. Two cohorts of 458 Italian Caucasian LOAD patients and 165 CAD patients were examined for the C-338A polymorphism and compared with respective control samples (260 and 106 subjects, respectively). The A allele was less present in LOAD patients than in controls, but an at limits statistically significant difference was achieved only in subjects aged less than 80 years, where only the AA genotypes appeared to have a protective role against the onset of the sporadic LOAD. For the overall CAD sample the pattern was similar and significant differences were observed only in subjects non carrying the apolipoprotein E (APOE) e*4 allele, where the A allele carrying genotypes had a protective role against the onset of the disease.

Different pattern of association of paraoxonase Gln192→Arg polymorphism with sporadic late-onset Alzheimer's disease and coronary artery disease

2003 ◽  
Vol 339 (1) ◽  
pp. 17-20 ◽  
Author(s):  
Renato Scacchi ◽  
Giuseppe Gambina ◽  
Maria Cristina Martini ◽  
Elisabetta Broggio ◽  
Teresio Vilardo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Coronary Artery Disease ◽  
Alzheimer's Disease ◽  
Coronary Artery ◽  
Late Onset ◽  
Artery Disease

Cortical senile plaques in coronary artery disease, aging and Alzheimer's disease

1990 ◽  
Vol 11 (6) ◽  
pp. 601-607 ◽  
Author(s):  
D.Larry Sparks ◽  
John C. Hunsaker ◽  
Stephen W. Scheff ◽  
Richard J. Kryscio ◽  
Jana L. Henson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Coronary Artery Disease ◽  
Alzheimer's Disease ◽  
Coronary Artery ◽  
Senile Plaques ◽  
Artery Disease
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