What is the clinical evidence from this study?

Study design: Case-Control. Population: Stable angina pectoris. Intervention: Stable angina pectoris vs. Normal subjects. Primary outcome: Maximal increases in intraplatelet cyclicAMP with PGE1 10(-4) M (%) (p=<0.01).

What question did this study set out to answer?

To examine whether impaired antiaggregating effects and intraplatelet cyclic AMP stimulation by prostaglandin E1 contribute to platelet hyperaggregability in stable angina pectoris.

June 1, 1995Journal of Cardiovascular Pharmacology

Impaired Responsiveness of Platelets from Patients with Stable Angina Pectoris to Antiaggregating and CyclicAMP-Elevating Effects of Prostaglandin E1

Q: What are the key findings of this study?

Platelets from patients with stable angina pectoris exhibited impaired responsiveness to PGE1, with significantly lower maximal cyclicAMP increases compared to normal subjects (220% vs 330%, p<0.01).

Q: What question did this study set out to answer?

To examine whether impaired antiaggregating effects and intraplatelet cyclic AMP stimulation by prostaglandin E1 contribute to platelet hyperaggregability in stable angina pectoris.

View Full Paper

Ask AI

Bookmark

Key result

Platelets from patients with stable angina pectoris exhibited impaired responsiveness to PGE1, with significantly lower maximal cyclicAMP increases compared to normal subjects (220% vs 330%, p<0.01).

Why the study?

Is the antiaggregating and cyclicAMP-elevating effect of PGE1 impaired in platelets from patients with stable angina pectoris compared to normal subjects?

Population

Platelets obtained from normal subjects and patients with stable angina pectoris

Comparison

Prostaglandin E1 added to platelet-rich plasma… vs Platelets from normal subjects

Design

Case-control

Authors

YCYuliy Y. Chirkov LCLarissa Chirkova RSRobert Sage

Discussion

Member takes

Overview

Impaired PGE1 responsiveness may link to platelet hyperaggregability in stable angina; hypothesis-generating and requires prospective confirmation before clinical consideration.

Key Points

To examine whether impaired antiaggregating effects and intraplatelet cyclic AMP stimulation by prostaglandin E1 contribute to platelet hyperaggregability in stable angina pectoris.
Measured ADP-induced aggregation and prostaglandin E1 (PGE1)-mediated reversal of incipient aggregation in platelet-rich plasma from normal subjects and patients with stable angina pectoris.
Quantified concentration-dependent intraplatelet cyclic AMP accumulation following exposure to PGE1.
The PGE1 concentration required for 50% reversal of aggregation (C50) was significantly higher in patients with stable angina (6.3 ± 1.6 × 10⁻⁷ M) than in normal controls (2.4 ± 0.3 × 10⁻⁸ M, p < 0.01).
Maximal intraplatelet cyclic AMP generation stimulated by 10⁻⁴ M PGE1 was significantly suppressed in angina patients (220 ± 20%) relative to normal subjects (330 ± 10%, p < 0.01).

Study Design

Type

Case-Control

Structured PICO

Is the antiaggregating and cyclicAMP-elevating effect of PGE1 impaired in platelets from patients with stable angina pectoris compared to normal subjects?

Population

Patients with stable angina pectoris and normal subjects evaluated for ex vivo platelet responsiveness to PGE1.

Exposure

Prostaglandin E1 (PGE1) added to platelet-rich plasma 0.5 min after ADP

Comparator

Platelets from normal subjects

Outcome

Concentrations of PGE1 associated with 50% reversal of aggregation (C50) and maximal increases in intraplatelet cyclicAMPsurrogate

Main Result

Absolute Event Rate: 220% vs 330%

p-value: p=<0.01

Patients with stable angina pectoris exhibit impaired platelet responsiveness to the antiaggregating and cyclicAMP-elevating effects of PGE1, which may contribute to platelet hyperaggregability in cardiovascular diseases.

Cite This Study

Chirkov et al. (1995) conducted a case-control in Stable angina pectoris. Stable angina pectoris vs. Normal subjects was evaluated on Maximal increases in intraplatelet cyclicAMP with PGE1 10(-4) M (%) (p=<0.01). Platelets from patients with stable angina pectoris exhibited impaired responsiveness to PGE1, with significantly lower maximal cyclicAMP increases compared to normal subjects (220% vs 330%, p<0.01).

synapsesocial.com/papers/6aa042eaca2b882a1e326bd9 https://doi.org/10.1097/00005344-199506000-00015

View Full Paper

Ask AI

Bookmark

June 1, 1995Journal of Cardiovascular Pharmacology

Impaired Responsiveness of Platelets from Patients with Stable Angina Pectoris to Antiaggregating and CyclicAMP-Elevating Effects of Prostaglandin E1

View Full Paper

Ask AI

Bookmark

Key result

Platelets from patients with stable angina pectoris exhibited impaired responsiveness to PGE1, with significantly lower maximal cyclicAMP increases compared to normal subjects (220% vs 330%, p<0.01).

Why the study?

Is the antiaggregating and cyclicAMP-elevating effect of PGE1 impaired in platelets from patients with stable angina pectoris compared to normal subjects?

Population

Platelets obtained from normal subjects and patients with stable angina pectoris

Comparison

Prostaglandin E1 added to platelet-rich plasma… vs Platelets from normal subjects

Design

Case-control

Authors

YCYuliy Y. Chirkov LCLarissa Chirkova RSRobert Sage

Discussion

Member takes

Overview

Impaired PGE1 responsiveness may link to platelet hyperaggregability in stable angina; hypothesis-generating and requires prospective confirmation before clinical consideration.

Key Points

To examine whether impaired antiaggregating effects and intraplatelet cyclic AMP stimulation by prostaglandin E1 contribute to platelet hyperaggregability in stable angina pectoris.
Measured ADP-induced aggregation and prostaglandin E1 (PGE1)-mediated reversal of incipient aggregation in platelet-rich plasma from normal subjects and patients with stable angina pectoris.
Quantified concentration-dependent intraplatelet cyclic AMP accumulation following exposure to PGE1.
The PGE1 concentration required for 50% reversal of aggregation (C50) was significantly higher in patients with stable angina (6.3 ± 1.6 × 10⁻⁷ M) than in normal controls (2.4 ± 0.3 × 10⁻⁸ M, p < 0.01).
Maximal intraplatelet cyclic AMP generation stimulated by 10⁻⁴ M PGE1 was significantly suppressed in angina patients (220 ± 20%) relative to normal subjects (330 ± 10%, p < 0.01).

Study Design

Type

Case-Control

Structured PICO

Is the antiaggregating and cyclicAMP-elevating effect of PGE1 impaired in platelets from patients with stable angina pectoris compared to normal subjects?

Population

Patients with stable angina pectoris and normal subjects evaluated for ex vivo platelet responsiveness to PGE1.

Exposure

Prostaglandin E1 (PGE1) added to platelet-rich plasma 0.5 min after ADP

Comparator

Platelets from normal subjects

Outcome

Concentrations of PGE1 associated with 50% reversal of aggregation (C50) and maximal increases in intraplatelet cyclicAMPsurrogate

Main Result

Absolute Event Rate: 220% vs 330%

p-value: p=<0.01

Cite This Study

synapsesocial.com/papers/6aa042eaca2b882a1e326bd9 https://doi.org/10.1097/00005344-199506000-00015

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

View Full Paper

Ask AI

Bookmark