The Adequacy of Subendocardial Oxygen Delivery

Brazier, John; Cooper, Norman; Buckberg, Gerald D.

doi:10.1161/01.cir.49.5.968

Cited by 140 publications

(16 citation statements)

References 33 publications

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“…During the collection of aortic flow, time to peak pressure and the relaxation times at 10, 50, and 80% total relaxation (RT 10, RT 50 , and RT 80 , respectively) were measured from the pressure traces. Systolic and diastolic pressure time integrals (STI, correlating with myocardial energy expenditure (31)(32)(33)(34), and DTI, correlating with diastolic function and coronary perfusion (35)(36)(37)(38)(39)(40)(41)(42), respectively) were calculated by integrating the systolic and diastolic portions of the pressure waves.…”

Section: Measurement Of Left Ventricular Pressure Development In Vivo-mentioning

confidence: 99%

“…Previous studies have established that the DTI/STI ratio correlates closely with the blood supply to the subendocardium (37)(38)(39)(40)(41)(42). Because coronary perfusion occurs during diastole, a faster rate of relaxation would produce a longer duration of diastole, yielding deeper perfusion from the coronary arteries.…”

Section: Regulation Of Ctni Function By Restrictedmentioning

confidence: 99%

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Proteolytic N-terminal Truncation of Cardiac Troponin I Enhances Ventricular Diastolic Function

Barbato

Huang

Hossain

et al. 2005

Journal of Biological Chemistry

131

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In the present study, we developed transgenic mice overexpressing the N-terminal truncated cTnI (cTnI-ND) in the heart to examine its biochemical and physiological significance. Ca 2؉ -activated actomyosin ATPase activity showed that cTnI-ND myofibrils had lower affinity for Ca 2؉ than controls, similar to the effect of isoproterenol treatment. In vivo and isolated working heart experiments revealed that cTnI-ND hearts had a significantly faster rate of relaxation and lower left ventricular end diastolic pressure compared with controls. The higher baseline relaxation rate of cTnI-ND hearts was at a level similar to that of wild type mouse hearts under ␤-adrenergic stimulation. The decrease in cardiac output due to lowered preload was significantly smaller for cTnI-ND hearts compared with controls. These findings indicate that removal of the N-terminal extension of cTnI via restricted proteolysis enhances cardiac function by increasing the rate of myocardial relaxation and lowering left ventricular end diastolic pressure to facilitate ventricular filling, thus resulting in better utilization of the Frank-Starling mechanism.

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Section: Measurement Of Left Ventricular Pressure Development In Vivo-mentioning

confidence: 99%

Section: Regulation Of Ctni Function By Restrictedmentioning

confidence: 99%

Proteolytic N-terminal Truncation of Cardiac Troponin I Enhances Ventricular Diastolic Function

Barbato

Huang

Hossain

et al. 2005

Journal of Biological Chemistry

131

View full text Add to dashboard Cite

show abstract

“…This progressive augmentation of coronary flow maintains overall myocardial oxygen delivery and occurs with a ~2-fold increase in MVO 2 and little/no change in myocardial oxygen extraction [10, 19, 34, 35, 47, 64, 67, 68]. However, evidence of enhanced myocardial lactate release and impairments to both sub-endocardial blood flow and cardiac contractile function have been reported with more severe reductions in hematocrit (≤ 10%) [1, 3, 37, 45, 64]. Earlier studies have suggested a role for reduced blood viscosity in the coronary response to anemia [5, 31, 33, 46, 62].…”

Section: Introductionmentioning

confidence: 99%

Regulation of myocardial oxygen delivery in response to graded reductions in hematocrit: role of K+ channels

et al. 2017

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This study was designed to identify mechanisms responsible for coronary vasodilation in response to progressive decreases in hematocrit. Isovolemic hemodilution was produced in open-chest, anesthetized swine via concurrent removal of 500 ml of arterial blood and the addition of 500 ml of 37°C saline or synthetic plasma expander (Hespan, 6% hetastarch in 0.9% sodium chloride). Progressive hemodilution with Hespan resulted in an increase in coronary flow from 0.39 ± 0.05 to 1.63 ± 0.16 ml/min/g (P < 0.001) as hematocrit was reduced from 32 ± 1% to 10 ± 1% (P < 0.001). Overall, coronary flow corresponded with the level of myocardial oxygen consumption, was dependent on arterial pressures ≥ ~60 mmHg, and occurred with little/no change in coronary venous PO2. Anemic coronary vasodilation was unaffected by the inhibition of nitric oxide synthase (L-NAME: 25 mg/kg iv; P = 0.92) or voltage-dependent K+ (KV) channels (4-aminopyridine: 0.3 mg/kg iv; P = 0.52). However, administration of the KATP channel antagonist (glibenclamide: 3.6 mg/kg iv) resulted in an ~40% decrease in coronary blood flow (P < 0.001) as hematocrit was reduced to ~10%. These reductions in coronary blood flow corresponded with significant reductions in myocardial oxygen delivery at baseline and throughout isovolemic anemia (P < 0.001). These data indicate that vasodilator factors produced in response to isovolemic hemodilution converge on vascular smooth muscle glibenclamide-sensitive (KATP) channels to maintain myocardial oxygen delivery and that this response is not dependent on endothelial-derived nitric oxide production or pathways that mediate dilation via KV channels.

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“…Uncontrollable renal anemia has a negative effect on maintaining the balance in myocardial oxygen supply and demand. In an animal study, it was reported that in the presence of even mild anemia in dogs, electrocardiographic signs of ischemia and relative subendocardial underperfusion were observed with aortic stenosis—a typical situation in which myocardial oxygen demand is increased [31]. This means that the combination of anemia with increased oxygen demand, such as hypertension and/or volume overload, readily leads to an imbalance in myocardial oxygen supply and demand.…”

Section: Imbalance In Myocardial Oxygen Supply and Demandmentioning

confidence: 99%

Ischemic Heart Disease in Patients with End-Stage Kidney Disease

Tanaka

Joki²,

Hase³

2015

Blood Purif

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Background: It was recently reported that the severity of coronary and carotid atherosclerosis in patients with end-stage kidney disease (ESKD) has improved over the last two decades. However, the frequency of coronary artery events observed at the initiation of dialysis remains high. Summary: Recently, 5 different clinical types of acute myocardial infarction (MI) were introduced in the third universal definition of MI. Type 2 MI, known as secondary MI, is a more heterogeneous entity, where a condition other than coronary artery narrowing contributes to an acute imbalance in oxygen supply and demand. In patients with chronic kidney disease, it has been demonstrated that type 2 MI is more common than type 1 MI, which is associated with coronary occlusive disease. It is suspected that patients with ESKD also often have type 2 MI. Factors associated with incremental increases in oxygen demand may cause myocardial ischemia in ESKD. Key Messages: Significant epicardial coronary narrowing might not be a necessary precursor of myocardial ischemia in ESKD. To prevent ischemic heart disease and improve prognosis in patients with ESKD, we need to pay attention not only to coronary stenotic lesions, but also to the factors associated with the induction of an imbalance in myocardial oxygen supply and demand.

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The Adequacy of Subendocardial Oxygen Delivery

Cited by 140 publications

References 33 publications

Proteolytic N-terminal Truncation of Cardiac Troponin I Enhances Ventricular Diastolic Function

Proteolytic N-terminal Truncation of Cardiac Troponin I Enhances Ventricular Diastolic Function

Regulation of myocardial oxygen delivery in response to graded reductions in hematocrit: role of K+ channels

Ischemic Heart Disease in Patients with End-Stage Kidney Disease

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