Circadian variation in occurrence of transient overt and silent myocardial ischemia in chronic stable angina and comparison with prinzmetal angina in men

Nademanee, Koonlawee; Intarachot, Vanida; Josephson, Martin A.; Singh, Bramah N.

doi:10.1016/0002-9149(87)90292-x

Cited by 121 publications

(25 citation statements)

References 16 publications

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“…Although our study population did not comprise a very large number of patients, the use of long-term electrocardiography over 48 hours certainly diminished the importance of evaluating only 39 patients. Regarding the findings of the long-term electrocardiography as a function of the distribution of ischemic events throughout the 24 hours of a day, we should first point out that the option of dividing the day into 4-hour intervals and for defining them from 11:00 pm to 3:00 am, from 3:00 am to 7:00 am and so on, was based on the previous experience of other authors 8,9,12,13,[15][16][17] , who reported, as a rule, a higher frequency of ischemic events from dawn until the first hours in the morning, the so-called circadian variation of ischemia, with or without symptoms. This evidence was based on studies that evaluated the incidence of acute myocardial infarction throughout the 24 hours of a day 18,19 , which showed a higher incidence between 3:00 am and 8:00 am.…”

Section: Discussionmentioning

confidence: 99%

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Does a circadian variation occur in myocardial ischemia over 48 hours in patients with unstable angina?

César¹,

Ferreira²,

Grupi³

et al. 2000

Arq. Bras. Cardiol.

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Section: Discussionmentioning

confidence: 99%

“…Reports exist indicating that ischemia, with or without symptoms, has a circadian variation in either stable 8,9 or unstable angina [10][11][12][13] . Moreover, we know neither the incidence of silent ischemia in individuals with unstable angina nor its variation throughout the 24 hours of a day in our patient population.…”

mentioning

confidence: 99%

Does a circadian variation occur in myocardial ischemia over 48 hours in patients with unstable angina?

César¹,

Ferreira²,

Grupi³

et al. 2000

Arq. Bras. Cardiol.

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“…ACE inhibitors had no effect on circadian HR rhythm, indicating that this drug class has little influence on the autonomic control of the heart as compared to Ca channel blockers or fl-blockers. The circadian rhythm of autonomic control of the heart could be an important underlying mechanism for the circadian distribution of cardiac events such as angina pectoris (Nademanee et al 1987) and transient myocardial ischemia (Rocco et al 1987). We speculate that Ca channel blockers, /3-blockers and ACE inhibitors may affect the prognosis of ischemic heart disease in different ways.…”

Section: Discussionmentioning

confidence: 99%

The Influence of Antihypertensive Agents on Circadian Rhythms of Blood Pressure and Heart Rate in Patients with Essential Hypertension.

Munakata

Imai

Hashimoto

et al. 1992

Tohoku J. Exp. Med.

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The effects of once-daily administration of calcium (Ca) channel blockers, R-blockers and angiotensinconverting enzyme (ACE) inhibitors on circadian rhythms of blood pressure (BP) and heart rate (HR) were studied using the cosinor method. Sixty-two recruited patients with essential hypertension (WHO stage I or II) were divided into three groups based on the class of administered drugs. In the Ca channel blocker group (n=37, age 54± 9.0 years), 18 patients were given YM 730 at a mean dose of 11± 4.0 mg/day (mean ± s.n. ), 8 were given nitrendipine (11 ± 6.7 mg/day), and 11 were given nisoldipine (8±6.4 mg/day). In the f3-blocker group (n=15, age 42+13.5 years), 13 patients were given atenolol (44+11.0 mg/day), 1 was given nadolol (30 mg/day), and 1 was given sustained-release propranolol (60 mg/day). In the ACE inhibitor group (n =10, age 56± 8.7 years), 7 patients were given enalapril (6± 2.8 mg/day), and 3 were given lisinopril (20 mg/day). Ambulatory BP monitoring (ABPM) was performed before and during treatment. Mean arterial pressure (MAP) and HR were monitored under ambulatory conditions every five minutes for 24 hr with a finger volume oscillometric device. In all three groups, the mesor of MAP decreased significantly, while the amplitude and acrophase did not change during treatment. /l-Blockers reduced the amplitude as well as the mesor of HR. Ca channel blockers increased the amplitude of HR without influencing the mesor. ACE inhibitors had no effect on the circadian rhythm parameters of HR. These results suggest that Ca channel blockers, /l-blockers and ACE inhibitors lowered BP throughout the day without changing the circadian BP rhythm. However, the three drug classes may have different influences on the autonomic nervous system that regulates circadian cardiac rhythm. circadian rhythm ; blood pressure ; heart rate ; antihypertensive agents ; essential hypertension

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“…11 Several investigators have proposed a role for vagal activation in coronary vasospasm. 12,13 However, some investigators have suggested that adrenergic activation, not vagal activation, is responsible, because of upregulation of vascular adrenergic receptors during low sympathetic activity during sleep. 14-18 Based on our results, the trend toward a decrease in the HF component before the onset of ischemia suggests that vagal withdrawal may be a factor involved in spontaneous coronary vasospasm in patients with variant angina.…”

Section: Time Changes In Autonomic Nervous Activitymentioning

confidence: 99%

Coronary Hyperreactivity to Adrenergic Stimulation and Increased Nocturnal Vagal Tone Trigger Coronary Vasospasm

et al. 1998

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The relationship between autonomic nervous system activity (ANA) and coronary vasoreactivity during transient myocardial ischemia was determined in patients with vasospastic angina (VA). ANA was measured by power spectral analysis of heart rate variability and humoral factors following intravenous infusion of insulin in 24 patients with VA and 6 control patients. Nine (38%) of the VA patients had significant ST segment depression (STD), and 4 of these patients had symptomatic STD. The frequency of anginal episodes in the 9 patients with VA and STD was significantly greater than that in the 15 VA patients without STD (3.4±3.1 vs 0.5±0.8 episodes/week, p<0.05). The increase in the LF/HF ratio 30 min after insulin injection in patients with STD was significantly greater than that in patients without STD (34±31% vs 4±34%, p<0.05). All of the patients with VA and STD had significant coronary vasospasm in response to the infusion of ≤20 g of acetylcholine, higher levels of nocturnal parasympathetic activity, and greater norepinephrine production in response to insulin stimulation than the VA patients without STD. These findings suggest that increased vagal tone and hyperreactivity to adrenergic stimulation may trigger vasospasm in patients with VA. (Jpn Circ J 1998; 62: 721 -726)

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Circadian variation in occurrence of transient overt and silent myocardial ischemia in chronic stable angina and comparison with prinzmetal angina in men

Cited by 121 publications

References 16 publications

Does a circadian variation occur in myocardial ischemia over 48 hours in patients with unstable angina?

Does a circadian variation occur in myocardial ischemia over 48 hours in patients with unstable angina?

The Influence of Antihypertensive Agents on Circadian Rhythms of Blood Pressure and Heart Rate in Patients with Essential Hypertension.

Coronary Hyperreactivity to Adrenergic Stimulation and Increased Nocturnal Vagal Tone Trigger Coronary Vasospasm

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