Myocardial Blood Flow in Pacing-Induced Angina (original) (raw)
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The relationship between myocardial blood flow and bradycardia in man
Cardiovascular Research, 1970
Authors' synopsis Myocardial blood flow was measured in patients with chronic complete heart block at each patient's idioventricular rate and at a paced rate of 80 and roolmin. Myocardial flow was found to be positively related to the increase in heart rate and a possible mechanism for this is suggested. Although much is known about the relationship between myocardial blood flow (MBF) and heart rates in excess of normal, less is known about MBF at abnormally low heart rates. There have been acute studies, in animals, when bradycardia has been induced by surgical section of the bundle of His (Starzl, Gaertner, and Baker, 1955) and in man, by Gregory, Mueller, Ayres, Gianelli, and Grace (1967) who studied the relationship between MBF, measured by the 1311 antipyrine infusion method, and heart rates varying from 4o-r4o/min in patients treated for complete heart block by electrical pacemaking. We have investigated the relationship between MBF and bradycardia in five patients with chronic complete heart block who were in a stable haemodynamic state for several months before investigation. Measurements of MBF were made by an improved nitrous oxide clearance technique (Hedworth-Whitty, Housley, and Abraham, 1969) at each patient's idioventricular rate (IVR) and at paced rates of 80 and roo/min. Patient selection Four males and one female, aged 62-72 yr, were studied when they underwent a trial of transvenous electrical pacemaking; each subject understood the nature of the study and con-This work was supported by a grant from the Sheldon Research Fund of the Birmingham Regional Hospital Board; also by the Endowment Fund of the United Birmingham Hospitals and the
On the distribution of myocardial flow
Basic Research in Cardiology, 1974
The regional myocardial blood flow distribution was studied in dogs using the tracer microsphere distribution method. Under normal hemodynamic conditions the endocardial layers received more blood than the epicardial layers. After acute but controlled coronary stenosis, the blood flow to the poststenotic area was found to be unchanged, or only slightly decreased when the diastolic coronary to aortic pressure ratio was not lower than 70%. When dipyridamole was injected during coronary stenosis, the myocardial flow became non-homogeneous.
Progressive vasomotor changes in ischaemic myocardium
Acta medica Scandinavica. Supplementum, 1985
Under certain conditions, a progressive increase in vascular resistance occurs within ischaemic myocardium during the first three hours after coronary artery stenosis. Measurements of vasodilator reserve in the ischaemic region demonstrated that this is at least partly due to an increase in vascular smooth muscle tone. Two hypotheses were suggested as an explanation: release of vasoconstrictors within the ischaemic area, or a decreasing release of vasodilators. Potential coronary constrictors considered included norepinephrine, PGF2 alpha, thromboxane A2, and high K+. Each of these substances was eliminated as the source of the vasoconstriction by pharmacological studies on ischaemic canine hearts. Measurement of adenosine release from isolated guinea pig hearts provided support for the possibility that the vasoconstriction results from a decreasing release of metabolic vasodilators. Throughout the period of ischaemia, both blood flow and myocardial function were far below the level...
Circulation, 1980
We developed a radioimmunoassay for plasma thromboxane B,, the metabolite of the coronary vasoconstrictor thromboxane A,. To see if thromboxane A, is produced during myocardial ischemia, we used atrial pacing to study 14 patients with greater than 75% occlusive coronary artery disease proved by arteriography. Paired samples were taken from the coronary sinus (CS) and an artery (A) for lactate and thromboxane B, analysis before pacing. During and after pacing at 140 beats/min, sampling was repeated. Before, during, immediately after and 10 minutes after pacing, percent myocardial lactate extractions (A-CS/A X 100) were 29.3 ± 3.7%, -21.1 ± 12.8%, -74.3 ± 20.3% and 25.1 + 3.5%, respectively (all changes p < 0.01). Before pacing, five patients had detectable coronary sinus or arterial thromboxane levels. During pacing, 18% and 40% increases occurred in coronary sinus and arterial blood, respectively (0.8 ± 0.1 to 0.9 ± 0.2 pmol/ml, and 0.5 0.2 to 0.7 ± 0.2 pmol/ml). Immediately after pacing, increases of 204% and 132% occurred in the coronary sinus and arterial blood (p < 0.05), respectively (2.3 ± 0.9 pmol/ml and
Journal of The American College of Cardiology, 1991
PAOLOG.CAMICI.MD.FESC.FACC.PAOLO MARRACCINI.MD. ROBERTO LORENZONI. MD. GIUSEPPE BUZZIGOLI. NEDA PECORI. ARMANDOPERISSINOTTO.ELEUTERIOFERRANNINI.MD. ANTONIO L'ABBATE. MD, FESC. FACC. MARIO MARZILLI. MD Pisu. I,",? Coronary hemrdynamics, m~ocardiil nxt&olism and kft VP". trkukr func,ton s, rest and aWr incremenlal artat paring were e*slus,ed ia I2 pattcnts H,,b s,Rss-b&cd qins and ST nogmm, depression, nngtagraphieatly ~rmal coronary artwier and no evidenre of spasm. generatJy labpkd as syndrome X. and in 10 normal subjuts. A, bmelillp sludv, erect cardiac vtin Row WI commwabk in patknts and control subjecls. Durtng pacing, M o&km r&epru"~ pmduc, wps r-bnl in the ,uo pupa, but thr rtop or the r&tin between rate-pr~ure prrdurt md grea, ~ardttc rein Row ws slgnblrantly kss skep in pfdknts thnn in normal subjects (O.WJ27 vs. O.OOSd mt/mm Hglwat, p < 0.0011. Nevorthelesr, the kfl ventrkukr ejpaton irsction was romparable in b+th grwps 8, re%,66f 6% ~7, L 'I%,,, = NS,sndduriqpaeio~V,~ 71. VS. 66 * 5%. p = NS,.
The American Journal of Cardiology, 1986
Numerous hemodynamic, electrocardiographic, metabolic and radionuclide measurements in various subsets of patients with coronary artery disease (CAD) reveal that ischemia does not always occur on the basis of increases in myocardial oxygen consumption. Continuous hemodynamic monitoring indicates that most episodes of myocardial ischemia are not preceded by increases in such major determinants of oxygen consumption as heart rate or blood pressure, but that these usually increase in response to the development of ischemia. The development of pain during ischemia is a late feature and most episodes are silent. There are no significant differences in the hemodynamic characteristics of symptomatic versus asymptomatic episodes of myocardial ischemia in patients with angina at rest or between those associated with ST-segment depression and those with ST-segment elevation. Continuous Holter recordings analyzed by compact analog technique in hospitalized and ambulatory patients with ischemic heart disease indicate that in both unstable and chronic stable angina, over two-thirds of myocardial ischemic episodes are clinically silent. Symptomatic and silent episodes do not differ significantly with respect to duration. Most symptomatic and asymptomatic episodes are not triggered by increases in the determinants of oxygen demand. Such episodes may arise on the basis of a critical reduction in the lumen of the diseased coronary artery leading to a primary reduction in blood flow. Intermittent obstruction due to changes in coronary vasomobility or possibly formation of thrombi may be a common mechanism for the pathogenesis of myocardial ischemia in patients with a varying spectrum of coronary artery lesions. At present, the precise clinical and prognostic significance of silent ischemia in CAD is not completely defined.(ABSTRACT TRUNCATED AT 250 WORDS)
The American Journal of Cardiology, 1983
Atrial pacing has been used to assess the physiologic impact of coronary artery disease (CAD). Several variables have served as markers of pacing-induced myocardial ischemia, but their specificities and sensitivities are unknown. Accordingly, in 28 patients, incremental atrial pacing was performed. Of the 28, 10 had no CAD. The left ventricular ejection fraction (LVEF) (by gated equilibrium blood pool scintigraphy) increased in this group (0.60 +/- 0.11 [mean +/- standard deviation] before pacing to 0.67 +/- 0.13 at peak-pacing, p = 0.002). In no patient did left ventricular end-diastolic pressure increase by greater than 5 mm Hg. No patient had lactate production, and 2 (20%) had electrocardiographic S-T segment depression greater than or equal to 0.1 mV. Four (40%) had chest pain with atrial pacing. In the remaining 18 patients with CAD, atrial pacing caused a decrease in LVEF greater than or equal to 0.05 (0.46 +/- 0.10 to 0.33 +/- 0.09, p less than 0.001) and new segmental wall motion abnormalities in all, indicating pacing-induced myocardial ischemia. Only 8 (44%) had an increase in left ventricular end-diastolic pressure of greater than 5 mm Hg, and only 9 (50%) had lactate production. Ten (56%) had ischemic electrocardiographic changes, and 12 (67%) had chest pain. Thus, the electrocardiographic, metabolic, and hemodynamic alterations that may accompany pacing-induced ischemia are specific but relatively insensitive markers of ischemia. In contrast, chest pain during atrial pacing is a nonspecific occurrence, appearing with similar frequency in normal subjects and patients with CAD and pacing-induced ischemia.
Reduction of pacing-induced myocardial ischemia by intravenous magnesium sulfate
The American Journal of Cardiology, 1995
M agneslum sulfate (MgSO4) has been widely used in the last decades as treatment for supraventrlcular or ventricular arrhythmias, l,2 particularly in patients with coronary artery disease 3-6 Because a sustmned increase In heart rate during tachyarrhythmlas may provoke symptomatic or asymptomatic myocardial ~schemla in these patients, we thought it would be of interest to investigate whether this drug could also prevent myocardml ischemm associated with increased myocardial oxygen requirements. This is also in light of previous observations showing that MgSO 4 may beneficially affect myocardial oxygen supply/demand ratio by coronary vasodilatatlon, 7-1° probably due to its calcium antagonist effects. H Thus, we investigated whether MgSO 4 can reduce myocardial ischemia in response to atrial pacing m patients with fixed coronary artery disease and stable angma e e • Eleven patients (10 men and 1 woman, mean age 54.1 + 11 years [range 38 to 67]) were studied during diagnostic coronary arteriography. underlines the most prominent chnical and anglograptuc findings. All patients had stable effort angma, defined by typical symptoms on exercise and a positive treadmill stress test result at a rate-pressure product that was reproducible (5: 20%) m repeated stresses We excluded patients with hypotension, recent (<6 months) myocardml infarction, left bundle branch block, atnoventricular block, and left ventncular ejection fraction <30% All patients had slgmficant coronary artery disease defined as the presence of a >70% stenosis m 1 of the major coronary arteries. Four of the 5 patients with occluded left anterior descending artery (patients 1, 2, 4, and 11) had good collaterals to the distal vessel. Left ventrlcular wall moaon was evaluated m the right anterior oblique projection and qualitatively analyzed according to a severity score that assigned I pomt to each segmental hypokmesla, 2 to segmental akmesla, and 3 to segmental dyslonesia or aneurysm. All drugs were discontinued at least 5 half-hves before the morning of the study. The study protocol was approved by the Committee for Chnlcal Research of the University of Naples School of Medicine Informed consent was obtained from each pauent.
Hemodynamic Effect of Myocardial Bridging
Circulation: Cardiovascular Interventions, 2009
M yocardial bridging with systolic milking is a frequent finding during coronary angiography. 1 Classically, it is considered a benign congenital anomaly because myocardial perfusion occurs in diastole. Milking is limited to systole and should therefore not impair myocardial perfusion. However, this physiology-based evidence is contradicted by numerous cases of coronary thrombus formation and myocardial infarc-tion, in individuals with pathological findings none other than a myocardial bridging.
The role of heart rate in myocardial ischemia from restricted coronary perfusion
Journal of Electrocardiology, 2001
Despite many years of study, certain aspects of myocardial ischemia remain incompletely understood. One observation that motivated this study is that acute, complete occlusion produces elevations but never depression of the ST-segment potentials in electrocardiographic leads over the ischemic zone. Limited flow, on the other hand, leads to ST-segment depression, both in in situ experiments and during clinical stress tests. The prevailing biophysical theory of ischemia suggests that complete occlusion should produce at least transient ST-segment depression, a finding we have neither observed in our own studies nor uncovered in the literature. Our goal with these experiments was to understand the difference between complete occlusion and reduced coronary flow, specifically the behavior at the transition between the two. We have carried out experiments using isolated dog hearts with a cannulated left anterior descending artery suspended in a human shaped electrolytic tank. To create a range of ischemic conditions, we changed coronary flow rates both suddenly and in controlled sequences and varied the heart rate of the isolated heart. The main finding was that in the isolated heart preparation, epicardial ST-segment depression over the ischemic zone arose only under conditions of combined restricted flow and elevated heart rate. Reduced coronary flow alone never produced ST-segment depression. These findings suggest that heart rate and probably metabolic work create the conditions necessary for subendocardial ischemia that reduced flow alone cannot provoke. They furthermore suggest that the degree of ST-segment depression for a given restriction in coronary flow may depend on heart rate, which supports the notion of rate correction for clinical stress ECG testing.