Abnormal Longitudinal, Base-to-Apex Myocardial Perfusion Gradient by Quantitative Blood Flow Measurements in Patients With Coronary Risk Factors

Hernandez-Pampaloni, Miguel; Keng, Felix; Kudo, Takashi; Sayre, James; Schelbert, Heinrich R.

doi:10.1161/hc3001.093503

Cited by 74 publications

(35 citation statements)

References 32 publications

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“…20 In addition, a base-to apex perfusion gradient, similar to that described in patients with coronary risk factors, 21 could result in regional differences in myocardial blood flow in the setting of catecholamine-mediated microvascular dysfunction. This irregularity of the density of adrenoceptors in the LV combined with catecholamine-mediated microvascular dysfunction could create a wall motion similar to 'apical ballooning'.…”

Section: Discussionmentioning

confidence: 96%

Local Release of Catecholamines From the Hearts of Patients With Tako-Tsubo-Like Left Ventricular Dysfunction

Kume

Kawamoto

Okura

et al. 2008

Circ J

157

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ako-tsubo-like left ventricular (LV) dysfunction ischaracterized by a unique morphologic feature on the left ventriculography (LVG) and clinical features that include a predominance of elderly women, as well as a favorable prognosis. [1][2][3][4][5][6][7] The LV wall motion abnormality is localized to the LV apical region (LV apical ballooning), and improves within several weeks. Although tako-tsubolike LV dysfunction sometimes mimics myocardial infarction (MI) with respect to its symptoms and electrocardiographic (ECG) changes, it is quite different because there is a lack of organic epicardial coronary artery occlusion. Recent studies have shown that patients with this disease have evidence of exaggerated sympathetic activation, with plasma catecholamine levels several times higher than those in age-and sex-matched patients with Killip class III MI. 8 Therefore, catecholamines may play an important part in the occurrence of this entity. However, whether the catecholamines are released from cardiac sympathetic efferent neurons in patients with tako-tsubo-like LV dysfunction remains poorly understood, so the purpose of this study was to investigate evidence of local release of catecholamines from the heart in patients with tako-tsubo-like LV dysfunction. MethodsFive consecutive patients (3 females, 2 males) were examined. All had complained of chest pain/discomfort and were diagnosed with tako-tsubo-like LV dysfunction according to the following criteria: (1) LV wall motion abnormality at the apex on LVG; (2) ST-segment elevation or T-wave abnormality in at least 2 contiguous ECG leads; (3) no history of prior MI; (4) normal coronary angiogram (luminal narrowing <25% in all 3 coronary arteries). [1][2][3][4][5][6][7] The presence or absence of coronary risk factors, such as hypertension, hyperlipidemia, diabetes mellitus, and smoking were determined. The study protocol was approved by the Ethics Committee of Kawasaki Medical School, and written informed consent was given by each patient. LVG and coronary angiography (CAG) were performed by the femoral approach after intravenous infusion of 5,000 U heparin. The LV end-diastolic pressure was obtained following LVG. The LV ejection fraction was calculated by the area -length method. 9 After confirming the LV apical wall motion abnormality and normal CAG, sampling of blood for the measurement of plasma catecholamine levels was performed from the aortic root (Ao) and coronary sinus (CS). Plasma catecholamine levels were determined through high-performance liquid chromatography. Serum creatine kinase (CK) level was measured every 3 h after admission and the peak value was recorded. Patients received standard drug therapy (eg, diuretics or vasodilator therapy) according to the attending cardiologist's discretion. After 3 weeks, follow-up LVG were performed in the same way as before. ResultsThe median age of the patients was 76 years (range 71-78) and 60% were women (Table 1). The patients reported a variety of causes of emotional or physical stress (case 1: operation o...

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Section: Discussionmentioning

confidence: 96%

Local Release of Catecholamines From the Hearts of Patients With Tako-Tsubo-Like Left Ventricular Dysfunction

Kume

Kawamoto

Okura

et al. 2008

Circ J

157

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“…An explanation is that with progressive proximal diffuse or segmental narrowing of the proximal parent artery more than distally, proximal resistance at maximal flow may become higher than distal artery resistance such that the gradual longitudinal MBF gradient is reduced or eliminated, again depending on the severity of proximal or distal artery disease and extent of branch disease. 7,9,10 Alternatively, more structural proximal disease may impair downstream distal artery endothelial-mediated vasodilation thereby also reducing the longitudinal MBF gradient. Of further interest, the observed longitudinal MBF difference during hyperemic flows in cardiovascular risk individuals without evidence of epicardial structural disease was more pronounced than in those with structural CAD.…”

Section: Discussionmentioning

confidence: 99%

“…1,2,5,6 Conversely, functional and/or structural abnormalities of the coronary arterial wall may impair flow-mediated coronary vasodilation predominantly of the epicardial artery. [7][8][9][10] Such functional alterations or diffuse epicardial narrowing of the epicardial arteries, 7,9,11 commonly accompanied by an impairment of flow-mediated vasodilation, have been suggested as cause for a more recently described longitudinal decrease in myocardial perfusion or MBF during pharmacologically stimulated hyperemia. [7][8][9] Until recently, PET flow studies assessing the longitudinal base-to-apex MBF gradient during pharmacologic vasodilation did not provide information on the presence of structural coronary artery disease (CAD).…”

Section: Introductionmentioning

confidence: 99%

“…[7][8][9][10] Such functional alterations or diffuse epicardial narrowing of the epicardial arteries, 7,9,11 commonly accompanied by an impairment of flow-mediated vasodilation, have been suggested as cause for a more recently described longitudinal decrease in myocardial perfusion or MBF during pharmacologically stimulated hyperemia. [7][8][9] Until recently, PET flow studies assessing the longitudinal base-to-apex MBF gradient during pharmacologic vasodilation did not provide information on the presence of structural coronary artery disease (CAD). Thus, it remains uncertain how the presence or absence of structural alterations of the epicardial artery may affect the manifestation of an abnormal longitudinal, base-to-apex MBF gradient during higher coronary flows.…”

Section: Introductionmentioning

confidence: 99%

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Structural epicardial disease and microvascular function are determinants of an abnormal longitudinal myocardial blood flow difference in cardiovascular risk individuals as determined with PET/CT

Valenta

Quercioli

Vincenti

et al. 2010

Journal of Nuclear Cardiology

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Background. The aim of this study was to determine whether epicardial structural disease may affect the manifestation of a longitudinal decrease in myocardial blood flow (MBF) or MBF difference during hyperemia in cardiovascular risk individuals, and its dependency on the flow increase.Methods and Results. In 54 cardiovascular risk individuals (at risk) and in 26 healthy controls, MBF was measured with 13 N-ammonia and PET/CT in mL/g/min at rest and during dipyridamole stimulation. Computed tomography coronary angiography (CTA) was performed using a 64-slice CT of a PET/CT system. Absolute MBFs during dipyridamole stimulation were mildly lower in the mid-distal than in the mid-LV myocardium in controls (2.20 ± .51 vs 2.29 ± .51, P < .0001), while it was more pronounced in at risk with normal and abnormal CTA (1.56 ± .42 vs 1.91 ± .46 and 1.18 ± .34 vs 1.51 ± .40 mL/g/min, respectively, P < .0001), resulting in a longitudinal MBF difference that was highest in at risk with normal CTA, intermediate in at risk abnormal CTA, and lowest in controls (.35 ± .16 and .22 ± .09 vs .09 ± .04 mL/g/min, respectively, P < .0001). On multivariate analysis, log-CCS and mid-LV hyperemic MBF increase, indicative of microvascular function, were independent predictors of the observed longitudinal MBF difference (P £ .004 by ANOVA).Conclusions. Epicardial structural disease and microvascular function are important determinants of an abnormal longitudinal MBF difference as determined with PET/CT. (J Nucl Cardiol 2010;17:1023-33.)

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“…In addition to the higher density of sympathetic nerves at the base of the heart than the apex [1], there is also evidence that apical myocardium has enhanced responsiveness to sympathetic stimulation, making the apex more susceptible to sudden surge in catecholamines [2]. Regional difference in myocardial blood flow could be due to the result of base to apex perfusion gradient described in patients with coronary risk factors [3].…”

mentioning

confidence: 99%

Response to: speculations on the pathophysiology of Takotsubo syndrome

Bathina

Weiss

Weintraub

2015

Expert Review of Cardiovascular Therapy

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Abnormal Longitudinal, Base-to-Apex Myocardial Perfusion Gradient by Quantitative Blood Flow Measurements in Patients With Coronary Risk Factors

Cited by 74 publications

References 32 publications

Local Release of Catecholamines From the Hearts of Patients With Tako-Tsubo-Like Left Ventricular Dysfunction

Local Release of Catecholamines From the Hearts of Patients With Tako-Tsubo-Like Left Ventricular Dysfunction

Structural epicardial disease and microvascular function are determinants of an abnormal longitudinal myocardial blood flow difference in cardiovascular risk individuals as determined with PET/CT

Response to: speculations on the pathophysiology of Takotsubo syndrome

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