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Biomedical subjects

M C Petch

Publications and source records attributed to M C Petch.

At least 37 records · Page 2Linked to original sources
PubMed1993

"Syndrome X" and coronary artery disease.

BACKGROUND: "Syndrome X" is a heterogeneous disorder that probably encompasses several disease states. The long-term prognosis in syndrome X is good, although a significant number of patients continue to experience chest pain and remain functionally limited. Several studies have reported that the development of coronary artery disease in patients with syndrome X is rare. Our experience, however, has shown that patients diagnosed as having syndrome X may develop atherosclerotic coronary artery disease over a relatively short period of time. METHODS: Three patients with syndrome X were studied with repeat coronary angiography. RESULTS AND CONCLUSIONS: We describe the development of coronary artery disease in three syndrome X patients over a relatively short time after their normal coronary angiogram. Accordingly, the physician should remain alert to this possibility.

Adult↗
PubMed1993

Effect of hyperventilation and mental stress on coronary blood flow in syndrome X.

OBJECTIVES: To assess the effect of hyperventilation and mental stress on coronary blood flow and symptom production in patients with syndrome X. DESIGN: A prospective study. Hyperventilation and mental stress tests were performed on the ward and were repeated in the cardiac catheter laboratory where coronary blood flow velocity was also measured with an intracoronary Doppler catheter in the left anterior descending coronary artery. Oesophageal manometry studies were also performed. PATIENTS: 29 patients with syndrome X (typical anginal chest pain, a positive exercise test, and normal coronary angiogram). SETTING: A regional cardiothoracic centre. RESULTS: Hyperventilation produced typical chest pain in 16 patients on the ward. 13 patients experienced their typical chest pain with mental stress test 5. Ten patients experienced chest pain with both hyperventilation and mental stress tests. This pattern was reproduced exactly when the tests were repeated in the cardiac catheter laboratory. Hyperventilation produced a significant increase in the rate-pressure product during ward and laboratory testing. There was, however, no significant change in the rate-pressure product on mental stress tests. The mean (SEM) coronary flow velocity decreased significantly on hyperventilation in the catheter laboratory from 10.0 (0.92) cm/s to 5.9 (0.72) cm/s (p < 0.001). There was also a significant reduction in the mean (SEM) coronary blood flow velocity on mental stress tests from 9.8 (0.86) cm/s to 7.4 (0.6) cm/s (p < 0.001). This reduction in flow velocity occurred in the absence of any changes in diameter of the left anterior descending artery. Further analysis showed that the coronary flow velocity was reduced significantly in only that group of patients in which hyperventilation and mental stress provoked chest pain. There was a significant increase in the arterial concentrations of noradrenaline on both hyperventilation and mental stress testing. Oesophageal manometry showed abnormalities in 17% of patients. CONCLUSIONS: Both hyperventilation and mental stress can produce chest pain in patients with syndrome X and this is associated with a reduction in coronary blood flow velocity. The results of this study suggests that this reduction in coronary flow occurs as a result of increased microvascular resistance.

Adult↗
PubMed1993

Clinical presentation and functional prognosis in syndrome X.

OBJECTIVES: To assess the effect of clinical presentation on functional prognosis in patients with syndrome X. DESIGN: A prospective study. Patients with syndrome X presenting with unstable angina and stable angina were followed up with a questionnaire to examine their functional state. PATIENTS: 41 patients with syndrome X and unstable angina and 41 patients with syndrome X and stable angina. Syndrome X was defined as typical anginal chest pain, a positive exercise test, and normal coronary angiogram. SETTING: Regional cardiothoracic centre. RESULTS: The mean follow up time was 36 (range 20-51) months for the unstable angina group and 35 (range 19-51) months for the stable angina group. No patient was lost to follow up in either group. At follow up 28 patients in the unstable angina group were pain free compared with 15 patients in the stable angina group (p = 0.008). Seven patients in the unstable angina group had further hospital admission with chest pain after the cardiac catheterisation compared wtih 12 patients in the stable angina group (NS). Seven patients in the unstable angina group believed that they had heart disease compared with 27 in the stable angina group (p < 0.001). 26 patients in the unstable angina group but only eight patients in the stable angina group were unlimited in their physical activity (p < 0.001). 12 patients in the unstable angina group compared with 27 patients in the stable angina group were unable to work normally because of chest pain (p < 0.001). The mean (SD) duration of symptoms before cardiac catheterisation was 7.9 (4.7) months in the unstable angina group and 13.4 (5.6) months in the stable angina group (p < 0.001). 10 patients in the unstable angina group and 24 patients in the stable angina group still attended hospital outpatient clinics because of chest pain (p = 0.004). 16 patients in the unstable angina group and 29 patients in the stable angina group were still taking regular antianginal medication (p < 0.001). CONCLUSIONS: Patients with syndrome X who present with unstable angina have a significantly better functional prognosis than those presenting with symptoms of stable angina. This may reflect differences in underlying pathophysiological mechanisms.

Adult↗
PubMed1993

Coronary flow reserve measurements with a new Judkins-style Doppler angiographic catheter.

The authors assessed whether measurements obtained by Judkins-style Doppler catheters are comparable to those achieved with the intracoronary Doppler technique in 42 patients with normal coronary arteries on angiography (19 syndrome X and 23 heart transplant patients). Resting coronary flow velocity and response to a hyperemic intracoronary dose of papaverine was measured with a Judkins-style, 8F Doppler-tipped catheter positioned in the left coronary ostium and a 3.6F intracoronary Doppler catheter positioned in the proximal left anterior descending artery. Mean coronary flow velocity at rest was significantly higher with the Judkins Doppler (10.1 +/- 4.6 vs 6.3 +/- 4.5 cm/sec, p < 0.01). The mean coronary flow velocity at peak hyperemia was also significantly higher with the Judkins Doppler (33.7 +/- 14.1 vs 19.7 +/- 11.5 cm/sec, p < 0.01). Coronary flow reserve was 3.57 +/- 1.3 with the Judkins Doppler and 3.47 +/- 1.2 with the intracoronary Doppler (r = 0.85). A second study was performed in 14 heart transplant patients with the intracoronary Doppler positioned in the left main coronary artery. The resting and hyperemic flow velocities were again higher with the Judkins Doppler but the differences were not statistically significant. There was again a strong correlation between the Doppler catheters for coronary flow reserve measurements. The Judkins-style Doppler technique appears to be a quick, safe, and accurate alternative to the intracoronary Doppler technique.

Cardiac Catheterization↗
PubMed1991

In vivo demonstration of cardiac beta 2-adrenoreceptor sensitization by beta 1-antagonist treatment.

Treatment with beta 1-selective antagonists causes selective sensitization of isolated strips of human atrial myocardium to the inotropic action of epinephrine and beta 2-agonists but not of norepinephrine. To determine whether beta 1-selective antagonist treatment alters the responsiveness of cardiac beta 2-adrenoreceptors in vivo, we measured the positive chronotropic responses to salbutamol injected into the right coronary artery. Ten patients treated with atenolol (50-100 mg daily) were compared with 10 patients not treated with beta-blockers. The mean dose required to cause an increase in heart rate of 30 beats/min was 2.29 micrograms (log dose 0.36 +/- 0.12 micrograms [mean +/- SEM]) in the atenolol-treated patients. In the non-beta-blocker-treated patients, the dose required to cause an increase in heart rate of 30 beats/min was significantly greater, 8.91 micrograms (log dose 0.95 +/- 0.11 micrograms) (p less than 0.005). We conclude that treatment with beta 1-selective beta-blockers leads to increased cardiac responsiveness to beta 2-adrenoreceptor stimulation. This may be the underlying mechanism of the beta-blocker withdrawal syndrome and may make the heart more susceptible to the adverse effects of epinephrine in situations of stress (e.g., myocardial infarction).

Adrenergic beta-Antagonists↗
PubMed1990

Lawnmower angina.

Explore the source record for details and available documents.

Activities of Daily Living↗
PubMed1989

Intracoronary injections of salbutamol demonstrate the presence of functional beta 2-adrenoceptors in the human heart.

To demonstrate the presence of functional cardiac beta 2-adrenoceptors in man, we studied the responses to intracoronary injections of salbutamol in three groups of six patients. We injected salbutamol, a selective beta 2-adrenoceptor agonist, into the right coronary artery to avoid peripheral vasodilator action and to stimulate the sinoatrial node directly. Salbutamol injections caused a sinus tachycardia. The same doses of salbutamol injected into the aortic root caused no change in heart rate, ruling out a systemic effect. The mean dose required to cause an increase in heart rate of 30 beats/min (IHR30) was 2.6 micrograms in the first group of six patients. In 12 other patients salbutamol was given after beta-blockade to confirm the beta 2-selectivity of the responses. Doses of practolol (beta 1-selective blockade) and of propranolol (beta 1- and beta 2-blockade) that had equal beta 1-blocking activity were used. In six patients who were given practolol, the mean IHR30 dose was 2.1 micrograms. In six patients who were given propranolol, the mean IHR30 dose was significantly greater at 64 micrograms (p less than 0.001, practolol vs. propranolol). This study demonstrates that direct cardiac beta 2-adrenoceptor stimulation in man has a positive chronotropic effect.

Albuterol↗
PubMed1988

Heart block and paragonimiasis.

Intracardiac granulomas can cause complete heart block. A case of complete heart block is reported in a patient who had had paragonimiasis 30 years before and who had radiographic evidence of calcified granulomas in the heart and lungs.

Calcinosis↗