Differential impact of systolic and diastolic blood pressure level on JNC-VI staging. Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.
(57/2997)
The sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure classifies blood pressure into stages on the basis of both systolic (SBP) and diastolic (DBP) blood pressure levels. When a disparity exists between SBP and DBP stages, patients are classified into the higher stage ("up-staged"). We evaluated the effect of disparate levels of SBP and DBP on blood pressure staging and eligibility for therapy. We examined 4962 Framingham Heart Study subjects between 1990 and 1995 and determined blood pressure stages on the basis of SBP alone, DBP alone, or both. After the exclusion of subjects on antihypertensive therapy (n=1306), 3656 subjects (mean age 58+/-13 years; 55% women) were eligible. In this sample, 64.6% of subjects had congruent stages of SBP and DBP, 31.6% were up-staged on the basis of SBP, and 3.8% on the basis of DBP; thus, SBP alone correctly classified JNC-VI stage in approximately 96% (64.6%+31.6%) of the subjects. Among subjects >60 years of age, SBP alone correctly classified 99% of subjects; in those +info)
Hypotension in patients with coronary disease: can profound hypotensive events cause myocardial ischaemic events?
(58/2997)
OBJECTIVE: To determine whether anginal episodes might be related to extremes of hypotension in patients with ischaemic heart disease taking drugs to treat angina and heart failure. DESIGN AND SETTING: Observational study of patients with ischaemic heart disease attending an urban tertiary referral cardiology centre. INTERVENTIONS AND OUTCOME MEASURES: A selected patient population was enrolled, having: angina on one or more hypotensive cardiovascular medications; hypotension on clinic or ambulatory measurement; and a resting ECG suitable for ambulatory monitoring. Patients had echocardiography, ambulatory blood pressure monitoring, and Holter monitoring. Hypotension induced ischaemic (HII) events were defined as episodes of ST segment ischaemia occurring at least one minute after an ambulatory blood pressure measurement (systolic/diastolic) below 100/65 mm Hg during the day, or 90/50 mm Hg at night. RESULTS: 25 suitable patients were enrolled, and 107 hypotensive events were documented. 40 ST events occurred in 14 patients, of which a quarter were symptomatic. Fourteen HII events occurred in eight patients, with 13 of the 14 preceded by a fall in diastolic pressure (median diastolic pressure 57.5 mm Hg, interquartile range 11, maximum 72 mm Hg, minimum 45 mm Hg), and six preceded by a fall in systolic pressure (chi(2) = 11.9, p < 0.001). ST events were significantly associated with preceding hypotensive events (chi(2) = 40.2, p < 0.0001). Patients with HII events were more frequently taking multiple hypotensive drug regimens (8/8 v 9/17, chi(2) = 5.54, p = 0.022). CONCLUSIONS: In patients with ischaemic heart disease and hypotension, symptomatic and silent ischaemia occurred in a temporally causal relation with hypotension, particularly for diastolic pressures, suggesting that patients with coronary disease may be susceptible to ischaemic events incurred as a result of low blood pressure caused by excessive hypotensive drug treatment. (+info)
Right ventricular diastolic function in patients with hypertrophic cardiomyopathy--an invasive study.
(59/2997)
To assess diastolic function of the right ventricle (RV) in patients with hypertrophic cardiomyopathy (HCM), biplane RV angiograms and RV pressures were analyzed in 19 HCM patients and in 13 normal subjects. RV and left ventricle (LV) pressures were measured using catheter-tip manometers. RV volumes were obtained from frame-by-frame tracings of angiograms. Ventricular relaxation was assessed by the time constant of isovolumic pressure decay (T). The peak filling rate (PFR) and the time to PFR (TPFR) were used as parameters of early diastolic filling, and the right atrial contribution to RV filling (%AF) was used as a parameter of late diastolic filling. The T for the RV was significantly prolonged in HCM patients. However, there was no significant correlation between the T for the RV and LV, nor did the T for the RV correlate with the RV ejection fraction or interventricular septal wall thickness. The TPFR, but not PFR, was significantly greater in HCM patients, and the %AF tended to be increased in HCM, but not significantly. The RV diastolic pressure-volume relations in the HCM patients shifted upward. In conclusion, impaired isovolumic relaxation and delayed diastolic filling and decreased diastolic distensibility are present in the RV of HCM patients. (+info)
Analytical expression of effective afterload in aortic and mitral regurgitation.
(60/2997)
Effective arterial elastance (Ea) is the coupling parameter between the left ventricle and peripheral circulation in normal subjects. If left ventricular end systolic pressure (Pes), contractility (Es) and Ea are known, left ventricular end diastolic volume (LVEDV) and ejection fraction of the ventricle are completely determined. The aim of this study was to give an analytical expression for Ea in patients with mitral and aortic regurgitation, and predict both LVEDV and the effect of vasodilator therapy on LVEDV. Twenty-three subjects with atypical chest pain, 15 patients with mitral insufficiency and 11 with aortic insufficiency underwent diagnostic cardiac catheterization, coronary angiography, and left ventricular cineangiography, which was analyzed quantitatively. Ea was 2.05 +/- 0.63 in normal subjects, while it was 1.28 +/- 0.71 and 1.57 +/- 0.87 in patients with mitral and aortic insufficiency, respectively. All these groups differed with ANOVA test (p = 0.0031). We tested the ability of the analytical expressions for Ea in normal subjects, and patients with mitral insufficiency or aortic insufficiency to predict measured Ea and LVEDV. Ea and LVEDV were predicted rather accurately in every case (p < 0.0001). We used published data to test the effect of resistance modulation on LVEDV. Predicted and measured LVEDV were linearly correlated both in aortic (p < 0.0001) and mitral insufficiency (p = 0.027). Moreover, in some cases a left ventricular enlargement after vasodilator therapy could be anticipated because of an unbalanced decrease in resistance and heart rate. Ea seems to be the coupling parameter between the left ventricle and the peripheral circulation not only in normal subjects, but also in patients with mitral or aortic regurgitation; its measurement before administering vasodilating drugs may be useful in order to predict the effects on LVEDV, and achieve an optimal ventriculoarterial coupling. (+info)
Acute right ventricular restrictive physiology after repair of tetralogy of Fallot: association with myocardial injury and oxidative stress.
(61/2997)
BACKGROUND: Acute right ventricular (RV) restrictive physiology after tetralogy of Fallot repair results in low cardiac output and a prolonged stay in the intensive care unit (ICU). However, its mechanism remains uncertain. METHODS AND RESULTS: In the first 24 hours after tetralogy of Fallot repair (n=11 patients), serial prospective measurements were performed of cardiac troponin T, indexes of NO production (NO(2)(-) and NO(3)(-) combined as NOx), and iron metabolism and antioxidants. RV diastolic function was assessed by transthoracic Doppler echocardiography. Patients who had a long stay in the ICU were characterized by restrictive RV physiology (nonrestrictive group [n=7]: 3.0+/-0.6 days [mean+/-SD]; restrictive group [n=4]: 10.7+/-3.1 days). Troponin T peak concentration and the area under its concentration-time curve (AUC) were higher in the restrictive RV group (peak: restrictive group 17. 0+/-2.8 microg/L, nonrestrictive group 10.4+/-4.6 microg/L, P<0.03; AUC: restrictive group 268.8+/-73.6 microg. h(-1). L(-1), nonrestrictive group 136.2+/-48.3 microg. h(-1). L(-1), P<0.03). Plasma NOx/creatinine concentrations were higher in the restrictive group than the nonrestrictive group at 2 hours after bypass (restrictive group 1.3+/-0.4, nonrestrictive group 0.8+/-0.2; P=0. 04) but were similar by 24 hours. Iron loading peaked 2 to 10 hours after bypass and was more severe in the restrictive group (peak transferrin saturation: restrictive group 83.9+/-13.0%, nonrestrictive group 58.3+/-16.2%, P=0.05; minimum total iron-binding capacity: restrictive group 0.59+/-0.21%, nonrestrictive group 0.76+/-0.06%, P=0.04; minimum iron-binding antioxidant activity to oxyorganic radicals: restrictive group 9. 5+/-22.4%, nonrestrictive group 50.6+/-11.4%, P=0.01). CONCLUSIONS: After tetralogy of Fallot repair, acute restrictive RV physiology is associated with greater intraoperative myocardial injury and postoperative oxidative stress with severe iron loading of transferrin. (+info)
Specificity of synergistic coronary flow enhancement by adenosine and pulsatile perfusion in the dog.
(62/2997)
1. Coronary flow elevation from enhanced perfusion pulsatility is synergistically amplified by adenosine. This study determined the specificity of this interaction and its potential mechanisms. 2. Mean and phasic coronary flow responses to increasing pulsatile perfusion were assessed in anaesthetized dogs, with the anterior descending coronary artery servoperfused to regulate real-time physiological flow pulsatility at constant mean pressure. Pulsatility was varied between 40 and 100 mmHg. Hearts ejected into the native aorta whilst maintaining stable loading. 3. Increasing pulsatility elevated mean coronary flow +11.5 +/- 1.7 % under basal conditions. Co-infusion of adenosine sufficient to raise baseline flow 66 % markedly amplified this pulsatile perfusion response (+82. 6 +/- 14.3 % increase in mean flow above adenosine baseline), due to a leftward shift of the adenosine-coronary flow response curve at higher pulsatility. Flow augmentation with pulsatility was not linked to higher regional oxygen consumption, supporting direct rather than metabolically driven mechanisms. 4. Neither bradykinin, acetylcholine nor verapamil reproduced the synergistic amplification of mean flow by adenosine and higher pulsatility, despite being administered at doses matching basal flow change with adenosine. 5. ATP-sensitive potassium (KATP) activation (pinacidil) amplified the pulse-flow response 3-fold, although this remained significantly less than with adenosine. Co-administration of the phospholipase A2 inhibitor quinacrine virtually eliminated adenosine-induced vasodilatation, yet synergistic interaction between adenosine and pulse perfusion persisted, albeit at a reduced level. 6. Thus, adenosine and perfusion pulsatility specifically interact to enhance coronary flow. This synergy is partially explained by KATP agonist action and additional non-flow-dependent mechanisms, and may be important for modulating flow reserve during exercise or other high output states where increased flow demand and higher perfusion pulsatility typically co-exist. (+info)
Parvalbumin gene transfer corrects diastolic dysfunction in diseased cardiac myocytes.
(63/2997)
Heart failure frequently involves diastolic dysfunction that is characterized by a prolonged relaxation. This prolonged relaxation is typically the result of a decreased rate of intracellular Ca(2+) sequestration. No effective treatment for this decreased Ca(2+) sequestration rate currently exists. As an approach to possibly correct diastolic dysfunction, we hypothesized that expression of the Ca(2+) binding protein parvalbumin in cardiac myocytes would lead to increased rates of Ca(2+) sequestration and mechanical relaxation. Parvalbumin, which is normally absent in cardiac tissue, is known to act as a soluble relaxing factor in fast skeletal muscle fibers by acting as a delayed Ca(2+) sink. As a test of the hypothesis, gene transfer was used to express parvalbumin in isolated adult cardiac myocytes. We report here that expression of parvalbumin dramatically increases the rate of Ca(2+) sequestration and the relaxation rate in normal cardiac myocytes. Importantly, parvalbumin fully restored the relaxation rate in diseased cardiac myocytes isolated from an animal model of human diastolic dysfunction. These findings indicate that parvalbumin gene transfer offers unique potential as a possible direct treatment for diastolic dysfunction in failing hearts. (+info)
Coronary artery distensibility in diabetic patients with simultaneous measurements of luminal area and intracoronary pressure: evidence of impaired reactivity to nitroglycerin.
(64/2997)
OBJECTIVES: This study investigated whether noninsulin dependent diabetes mellitus (NIDDM) adversely affects the elastic properties of the coronary arteries in patients with coronary artery disease (CAD) and NIDDM. BACKGROUND: Attenuated vascular smooth muscle dilation to exogenous donors of nitric oxide, such as nitroglycerin, has been observed with forearm blood flow studies in patients with NIDDM. METHODS: Twenty patients with CAD and NIDDM (diabetics), and 20 patients with only CAD (nondiabetics) were evaluated. Intracoronary ultrasound (ICUS) imaging with simultaneous intracoronary pressure (P2) recordings were performed at the imaging site with 0.014 in fiber-optic high fidelity pressure monitoring wire. The same wire was used as guide wire for the ICUS catheter. Sites with less than 50% luminal stenosis by ICUS were studied. Recordings were done before and after 300 microg of intracoronary nitroglycerin (IC-NTG). Electrocardiographic tracings recorded simultaneously with ICUS images were used for timing. Systolic and diastolic cross-sectional lumen area (CSLA) and coronary artery distensibility (C-DIST) were measured, C-DIST = [(systolic CSLA-diastolic CSLA)/[(intracoronary pulse pressure) x (diastolic CSLA)]] x 1,000. RESULTS: Diabetics had smaller CSLA (diabetics = 8.6 +/- 0.6 mm2, nondiabetics = 11.5 +/- 0.5 mm2, p < 0.01). Although C-DIST was similar before IC-NTG in the two groups, it became significantly lower in diabetics after IC-NTG (diabetics C-DIST = 3.02 +/- 0.14 mm Hg(-1), nondiabetics C-DIST = 4.21 +/- 0.15 mm Hg(-1), p < 0.01). Degrees of circumference involved, total plaque burden and composition were similar in both groups. CONCLUSIONS: Noninsulin dependent diabetes mellitus reduces C-DIST after IC-NTG administration. (+info)