Effect of chronotropic and inotropic stimulation on the coronary pressure-flow relation in left ventricular hypertrophy

1997 ◽  
Vol 92 (4) ◽  
pp. 271-286 ◽  
Author(s):  
D. J. Duncker ◽  
R. J. Bache
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Pressure Flow ◽  
Coronary Pressure ◽  
Inotropic Stimulation

High-energy phosphate responses to tachycardia and inotropic stimulation in left ventricular hypertrophy

1994 ◽  
Vol 266 (5) ◽  
pp. H1959-H1970 ◽  
Author(s):  
R. J. Bache ◽  
J. Zhang ◽  
G. Path ◽  
H. Merkle ◽  
K. Hendrich ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
31P Nmr ◽  
Mechanical Performance ◽  
Systolic Pressure ◽  
Creatine Phosphate ◽  
High Energy ◽  
Left Ventricular ◽  
Subendocardial Ischemia ◽  
Inotropic Stimulation

Spatially localized nuclear magnetic resonance (NMR) spectroscopy was used to examine the effect of tachycardia and inotropic stimulation on myocardial ATP, creatine phosphate (CrP), and inorganic phosphate (Pi) in animals with left ventricular hypertrophy (LVH). Studies were performed in eight normal dogs and seven dogs with moderate LVH produced by banding the ascending aorta. 31P-NMR spectra were obtained from five layers across the LV wall, while blood flow (BF) was measured with microspheres during control conditions, pacing at 200 and 240 beats/min, and during dobutamine infusion (Dob). Myocardial ATP and CrP levels were normal in the LVH hearts during control conditions. Pacing did not alter the transmural distribution of perfusion or the levels of CrP, ATP, and Pi in normal hearts. In contrast, in four of seven LVH hearts, pacing decreased the subendocardial/subepicardial (ENDO/EPI) BF ratio and caused depletion of CrP and appearance of Pi characteristic of ischemia in the subendocardium. Dob produced greater increases in the heart rate x LV systolic pressure product (RPP) and greater increases of Pi and decreases of CrP in LVH than in normal hearts; however, at comparable elevations of RPP the alterations of Pi and CrP were similar in both groups. Although Dob decreased the ENDO/EPI in LVH hearts, Dob-induced alterations in CrP and Pi were uniform across the LV wall. Increasing myocardial BF with adenosine or carbochromen did not reverse the alterations in Pi or CrP produced by Dob. We conclude that 1) ENDO perfusion abnormalities during tachycardia in LVH do produce ENDO subendocardial ischemia; 2) when the degree of augmentation of mechanical performance is considered, the metabolic changes induced by Dob were similar in normal and LVH hearts; 3) Dob-induced alterations in Pi and CrP were not related to inadequate perfusion, since increasing coronary BF did not reverse these changes; and 4) alterations of Pi and CrP during Dob infusion were not more prominent in the ENDO, indicating that the decreased ENDO/EPI flow did not cause ENDO ischemia but may reflect relatively lower O2 demands in this region during inotropic stimulation.

Left Ventricular Hypertrophy

2014 ◽  
Vol 19 (2) ◽  
pp. 11-15
Author(s):  
Steven L. Demeter
Keyword(s):  
Risk Factors ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular Mass Index ◽  
Medical Science ◽  
Careful Analysis ◽  
Left Ventricular ◽  
Hypertensive Disease ◽  
Accurate Analysis ◽  
Clear Explanation

Abstract The fourth, fifth, and sixth editions of the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides) use left ventricular hypertrophy (LVH) as a variable to determine impairment caused by hypertensive disease. The issue of LVH, as assessed echocardiographically, is a prime example of medical science being at odds with legal jurisprudence. Some legislatures have allowed any cause of LVH in a hypertensive individual to be an allowed manifestation of hypertensive changes. This situation has arisen because a physician can never say that no component of LVH was not caused by the hypertension, even in an individual with a cardiomyopathy or valvular disorder. This article recommends that evaluators consider three points: if the cause of the LVH is hypertension, is the examinee at maximum medical improvement; is the LVH caused by hypertension or another factor; and, if apportionment is allowed, then a careful analysis of the risk factors for other disorders associated with LVH is necessary. The left ventricular mass index should be present in the echocardiogram report and can guide the interpretation of the alleged LVH; if not present, it should be requested because it facilitates a more accurate analysis. Further, if the cause of the LVH is more likely independent of the hypertension, then careful reasoning and an explanation should be included in the impairment report. If hypertension is only a partial cause, a reasoned analysis and clear explanation of the apportionment are required.

The association of ankle brachial index with left ventricular hypertrophy and left ventricular mass index: the Dong-gu study

VASA ◽  
2013 ◽  
Vol 42 (4) ◽  
pp. 284-291 ◽  
Author(s):  
Seong-Woo Choi ◽  
Hye-Yeon Kim ◽  
Hye-Ran Ahn ◽  
Young-Hoon Lee ◽  
Sun-Seog Kweon ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Left Ventricular Mass ◽  
Ventricular Hypertrophy ◽  
Left Ventricular Mass Index ◽  
Ankle Brachial Index ◽  
Intima Media Thickness ◽  
Left Ventricular ◽  
Baseline Survey ◽  
Ventricular Mass Index ◽  
Ventricular Mass

Background: To investigate the association between ankle-brachial index (ABI), left ventricular hypertrophy (LVH) and left ventricular mass index (LVMI) in a general population. Patients and methods: The study population consisted of 8,246 people aged 50 years and older who participated in the baseline survey of the Dong-gu Study conducted in Korea between 2007 and 2010. Trained research technicians measured LV mass using mode M ultrasound echocardiography and ABI using an oscillometric method. Results: After adjustment for risk factors and common carotid artery intima-media thickness (CCA-IMT) and the number of plaques, higher ABIs (1.10 1.19, 1.20 - 1.29, and ≥ 1.30) were significantly and linearly associated with high LVMI (1.10 - 1.19 ABI: β, 3.33; 95 % CI, 1.72 - 4.93; 1.20 - 1.29 ABI: β, 6.51; 95 % CI, 4.02 - 9.00; ≥ 1.30 ABI: β, 14.83; 95 % CI, 6.18 - 23.48). An ABI of 1.10 - 1.19 and 1.20 - 1.29 ABI was significantly associated with LVH (1.10 - 1.19 ABI: OR, 1.35; 95 % CI, 1.19 - 1.53; 1.20 - 1.29 ABI: OR, 1.59; 95 % CI, 1.31 - 1.92) and ABI ≥ 1.30 was marginally associated with LVH (OR, 1.73; 95 % CI, 0.93 - 3.22, p = 0.078). Conclusions: After adjustment for other cardiovascular variables and CCA-IMT and the number of plaques, higher ABIs are associated with LVH and LVMI in Koreans aged 50 years and older.

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