Probable association between ziprasidone and worsening hypertension
ABSTRACT According to premarketing studies, at least 1% of ziprasidone-treated patients exhibited hypertension; however, this figure is not necessarily attributable to the drug. A PubMed/MEDLINE search yielded no articles describing hypertension as a possible adverse event associated with oral ziprasidone therapy. We describe a 53-year-old African-American woman with hypertension and schizophrenia whose blood pressure increased during ziprasidone therapy. She experienced no similar blood pressure increases during therapy with four other atypical antipsychotics. Her mean systolic blood pressure during ziprasidone treatment (158 mm Hg) was significantly higher than before (141 mm Hg) and after (135 mm Hg) treatment. Also, her mean diastolic blood pressure during ziprasidone treatment (88 mm Hg) was significantly higher than after treatment (79 mm Hg). Linear regression analysis demonstrated that the patient's systolic blood pressure increased significantly with ziprasidone dose (regression coefficient [B] = 0.22 mm Hg x day/mg, 95% confidence interval 0.10-0.34, p=0.001). Thus, after adjusting for the effect of antihypertensive doses, an increase of 40 mg/day in ziprasidone yielded an increase of 8.8 mm Hg in systolic blood pressure. For unknown (perhaps genetic) reasons, this patient may have been particularly sensitive to ziprasidone. Clinicians prescribing ziprasidone in patients with hypertension should be aware that their hypertension could worsen with the addition of ziprasidone. If this occurs, replacement of ziprasidone with a different antipsychotic should be considered.
- SourceAvailable from: Hilario Blasco-Fontecilla[Show abstract] [Hide abstract]
ABSTRACT: A recent Finnish study reported that long-term cumulative exposure to any antipsychotic treatment was related to lower mortality than was no drug exposure. We hypothesize that the antipsychotic 5-HT2A receptor blockade might protect from ischemic heart disease and buffer the deleterious metabolic effects of antipsychotics. The 5-HT2A receptor may be involved in vascular smooth muscle contraction, coronary artery spasms, platelet aggregation and thrombus formation. 5-HT2A receptor blockade might protect from ischemic heart disease by decreasing platelet aggregation and myocardium hypertrophy. Long-term follow-up studies are needed to clearly establish the long-term contribution of the various antipsychotic drugs to ischemic heart disease, and to explore our hypothesis that 5-HT2A receptor blockade may be protective for cardiovascular disease.Schizophrenia Research 06/2010; 119(1-3):160-3. DOI:10.1016/j.schres.2009.12.005 · 4.43 Impact Factor
Article: Planning for the optimal design of studies to personalize antipsychotic prescriptions in the post-CATIE era: The clinical and pharmacoepidemiological data suggest that pursuing the pharmacogenetics of metabolic syndrome complications (hypertension, diabetes mellitus and hyperlipidemia) may be a reasonable strategy[Show abstract] [Hide abstract]
ABSTRACT: The variability of individual responses reported by the CATIE study has raised awareness of the need to reconsider personalizing prescriptions of antipsychotic medications for the purpose of establishing the best antipsychotic for each individual patient. As atypical antipsychotics are widely prescribed for severe mental illnesses other than schizophrenia and side effects are largely independent from diagnosis, personalizing antipsychotic dosing may have important public health implications. This hypothesis article emphasizes that, whereas other psychiatric medications may cause weight gain, antipsychotics appear to have additional effects. Antipsychotics may have direct effects (not explained by obesity) on hypertension, diabetes mellitus and hyperlipidemia. The clinical and pharmacoepidemiological literature appears to suggest that (1) antipsychotics rarely increase blood pressure, with the probable exception of clozapine; (2) antipsychotics (particularly clozapine and olanzapine) may interfere with glucose metabolism in a (still unknown) direct way, independently of their effects on obesity; and (3) clozapine and olanzapine (and possibly quetiapine and low-potency typical antipsychotics) may directly cause hyperlipidemia, independently of their effects on obesity. This commentary focuses on the effect sizes and the time interval/event sequence of the direct influences of antipsychotics on blood pressure, glucose metabolism and lipid metabolism. Cross-sectional lipid studies may show antipsychotic effects. It is hypothesized that it may be easier to design studies focusing on these three aspects than to design pharmacogenetic studies focusing on antipsychotic-induced weight gain or metabolic syndrome, which require long-term follow-up.Schizophrenia Research 12/2007; 96(1-3):185-97. DOI:10.1016/j.schres.2007.05.020 · 4.43 Impact Factor