Acute Hemodynamic Effects Research Articles

Renal outcomes in hypertensive Black patients at high cardiovascular risk

The ACCOMPLISH trial (Avoiding Cardiovascular events through Combination therapy in Patients Living with Systolic Hypertension) was a 3-year multicenter, event-driven trial involving patients with high cardiovascular risk who were randomized in a double-blinded manner to benazepril plus either hydrochlorothiazide or amlodipine and titrated in parallel to reach recommended blood pressure goals. Of the 8125 participants in the United States, 1414 were of self-described Black ethnicity. The composite kidney disease end point, defined as a doubling in serum creatinine, end-stage renal disease, or death was not different between Black and non-Black patients, although the Blacks were significantly more likely to develop a greater than 50% increase in serum creatinine to a level above 2.6 mg/dl. We found important early differences in the estimated glomerular filtration rate (eGFR) due to acute hemodynamic effects, indicating that benazepril plus amlodipine was more effective in stabilizing eGFR compared to benazepril plus hydrochlorothiazide in non-Blacks. There was no difference in the mean eGFR loss in Blacks between therapies. Thus, benazepril coupled to amlodipine was a more effective antihypertensive treatment than when coupled to hydrochlorothiazide in non-Black patients to reduced kidney disease progression. Blacks have a modestly higher increased risk for more advanced increases in serum creatinine than non-Blacks.

Acute Beneficial Hemodynamic Effects of a Novel 3D-Echocardiographic Optimization Protocol in Cardiac Resynchronization Therapy

BackgroundPost-implantation therapies to optimize cardiac resynchronization therapy (CRT) focus on adjustments of the atrio-ventricular (AV) delay and ventricular-to-ventricular (VV) interval. However, there is little consensus on how to achieve best resynchronization with these parameters. The aim of this study was to examine a novel combination of doppler echocardiography (DE) and three-dimensional echocardiography (3DE) for individualized optimization of device based AV delays and VV intervals compared to empiric programming.Methods25 recipients of CRT (male: 56%, mean age: 67 years) were included in this study. Ejection fraction (EF), the primary outcome parameter, and left ventricular (LV) dimensions were evaluated by 3DE before CRT (baseline), after AV delay optimization while pacing the ventricles simultaneously (empiric VV interval programming) and after individualized VV interval optimization. For AV delay optimization aortic velocity time integral (AoVTI) was examined in eight different AV delays, and the AV delay with the highest AoVTI was programmed. For individualized VV interval optimization 3DE full-volume datasets of the left ventricle were obtained and analyzed to derive a systolic dyssynchrony index (SDI), calculated from the dispersion of time to minimal regional volume for all 16 LV segments. Consecutively, SDI was evaluated in six different VV intervals (including LV or right ventricular preactivation), and the VV interval with the lowest SDI was programmed (individualized optimization).ResultsEF increased from baseline 23±7% to 30±8 (p<0.001) after AV delay optimization and to 32±8% (p<0.05) after individualized optimization with an associated decrease of end-systolic volume from a baseline of 138±60 ml to 115±42 ml (p<0.001). Moreover, individualized optimization significantly reduced SDI from a baseline of 14.3±5.5% to 6.1±2.6% (p<0.001).ConclusionsCompared with empiric programming of biventricular pacemakers, individualized echocardiographic optimization with the integration of 3-dimensional indices into the optimization protocol acutely improved LV systolic function and decreased ESV and can be used to select the optimal AV delay and VV interval in CRT.

Inhaled treprostinil: a therapeutic review

Pulmonary arterial hypertension (PAH) is a life-threatening disease which, if untreated, leads to right ventricular failure and often death. Several effective therapies are now available for PAH, including endothelin receptor antagonists, phosphodiesterase-5 inhibitors, and prostacyclin analogs. The prostacyclin analog treprostinil has proven efficacious when delivered by subcutaneous or intravenous infusion, and most recently by inhalation. Inhaled treprostinil has been shown to be 64%–72% bioavailable in healthy volunteers. Pilot clinical studies have elucidated the acute hemodynamic effects and relative pulmonary selectivity of this agent, as well as established target dosing in PAH and nonoperable chronic thromboembolic PAH. Likewise, chronically administered inhaled treprostinil resulted in clinical and hemodynamic improvement. Both pilot studies confirmed a satisfactory safety profile in patients with PAH. The pivotal Phase III trial, TRIUMPH-I, demonstrated the efficacy and safety of inhaled treprostinil (target dose of 54 μg four times daily) in PAH patients added to background therapies of bosentan or sildenafil, as assessed by improvements in the primary endpoint, peak six-minute walk distance (median placebo-corrected treatment effect of 20 m), as well as select secondary endpoints. Inhaled treprostinil is approved by the US Food and Drug Administration for patients with World Health Organization Group I PAH to improve exercise ability. Studies establishing effectiveness included predominately patients with New York Heart Association functional class III symptoms and etiologies of idiopathic or heritable PAH (56%) or PAH associated with connective tissue diseases (33%).

Ophthalmic Artery Vasodilation after Intranasal Estradiol Use in Postmenopausal Women

The study aim was to evaluate the acute hemodynamic effects of intranasal 17-beta-estradiol on ophthalmic arterial circulation in postmenopausal women. Twenty-one healthy women in natural menopause for at least 6 months (mean age: 53.2± 2.9 years) were investigated. Each patient received 300 µg intranasal 17-beta-estradiol. We evaluated the heart rate, systolic and diastolic blood pressure, ophthalmic artery velocity at systolic and diastolic peak and its flow curve integral (FCI) before and 30, 60 and 180 minutes after the administration of the drug. At all time points, the ophthalmic artery FCI showed statistically significant variations (p<0.001) of velocity (cm/sec) compared to T0 (speed recorded at baseline before drug administration). Moreover, systolic blood pressure, diastolic blood pressure and heart rate did not significantly differ each other after drug administration. Administration of a single dose of intranasal 17-beta-estradiol to healthy postmenopausal women increases ophthalmic artery perfusion.

Comparison of Acute Hemodynamic Effects of Aerosolized Iloprost and Inhaled Nitric Oxide in Adult Congenital Heart Disease with Severe Pulmonary Arterial Hypertension

To compare the acute hemodynamic effects of aerosolized iloprost and inhaled nitric oxide (NO) in adult congenital heart disease (CHD) patients with severe pulmonary arterial hypertension (PAH). One hundred and eighty five adult CHDs with severe PAH were nonrandomized into two groups (iloprost, n=127; NO, n=58). Various hemodynamic parameters were measured before and after iloprost or NO inhalation. Iloprost and NO inhalation resulted in significant reductions in pulmonary arterial pressure (from 110.6±21.8 mmHg to 105.5±22.3 mmHg, p<0.05; from 113.1±18.7 mmHg to 107.2±19.9 mmHg, p<0.05, respectively) and pulmonary vascular resistance (PVR) (from 13.4±8.3 Wood units to 9.6±6.4 Wood units, p<0.01; from 13.7±7.1 Wood units to 9.3±4.9 Wood units, p<0.01, respectively) and increases in pulmonary blood flow (from 6.7±3.3 L/min to 9.4±5.8 L/min, p<0.05; from 6.6±3.1 L/min to 9.6±5.9 L/min, p<0.01, respectively) and the Qp/Qs ratio (from 1.5±0.8 to 2.1±1.4, p<0.01; from 1.5±0.8 to 2.0±1.3, p<0.01, respectively). When the effects of inhaled iloprost and NO were compared, similar reductions in pulmonary arterial pressure and pulmonary vascular resistance were observed. Aerosolized iloprost and inhaled nitric oxide (iNO) were generally well tolerated and no patient experienced any side effects during inhalation. Aerosolized iloprost can be effectively and safely used and might be an alternative to NO for testing pulmonary vascular reactivity and treating severe PAH in adult CHD patients.

Effects of high-fructose corn syrup and sucrose on the pharmacokinetics of fructose and acute metabolic and hemodynamic responses in healthy subjects

It is unclear whether high-fructose corn syrup (HFCS), which contains a higher amount of fructose and provides an immediate source of free fructose, induces greater systemic concentrations of fructose as compared with sucrose. It is also unclear whether exposure to higher levels of fructose leads to increased fructose-induced adverse effects. The objective was to prospectively compare the effects of HFCS- vs sucrose-sweetened soft drinks on acute metabolic and hemodynamic effects. Forty men and women consumed 24 oz of HFCS- or sucrose-sweetened beverages in a randomized crossover design study. Blood and urine samples were collected over 6 hours. Blood pressure, heart rate, fructose, and a variety of other metabolic biomarkers were measured. Fructose area under the curve and maximum concentration, dose-normalized glucose area under the curve and maximum concentration, relative bioavailability of glucose, changes in postprandial concentrations of serum uric acid, and systolic blood pressure maximum levels were higher when HFCS-sweetened beverages were consumed as compared with sucrose-sweetened beverages. Compared with sucrose, HFCS leads to greater fructose systemic exposure and significantly different acute metabolic effects.

Abstract 17487: S-Nitroso Human Serum Albumin (S-NO-HSA) Attenuates Pulmonary Hypertension, Improves Right Ventricular-Arterial Coupling and Reduces Oxidative Stress in a Chronic Right Ventricle Volume Overload Model

BACKGROUND The study was aimed to examine the acute overall hemodynamic and oxidative stress effects to intravenous S-NO-HSA infusion in a model of chronic left-to-right shunt-induced pulmonary arterial hypertension and right ventricle failure. METHODS AND RESULTS Fifty male Wistar rats underwent surgical creation of aorto-caval fistula (Qp/Qs&gt; 2.0) After 10 weeks they were randomly treated with S-NO-HSA (0.5 υmol/kg/h) (n. 20) or human serum albumin (HSA) (n. 25) infusion for 60 minutes. Right ventricular contractility, right ventriculo-vascular coupling and ventricular interdependence were assessed in vivo ad different preloads by biventricular conductance catheters prior and after 60 minutes infusion. Heart and lung biopsies were obtained to determine oxidative stress by reduced to oxidized glutathione (GSH/GSSG) ratio and high energy phosphates content. S-NO-HSA compared to HSA infusion resulted in a significant reduction in right ventricular afterload expressed by effective pulmonary arterial elastance (Ea) (0.49 +/- 0.3 versus 1.2 +/- 0.2 mmHg/ml; P = 0.0005). S-NO-HSA significantly improve right ventricular diastolic function (slope of end-diastolic pressure-volume relations) but not contractility (slope of preload recruitable stroke work), whereas a significant increase in the efficiency of ventricular-vascular coupling (ratio of end-systolic to pulmonary arterial elastances: Ees/Ea) occurred after S-NO-HSA but not HSA infusion (from 0.35 +/- 0.17 to 0.94 +/- 0.21; P = 0.005 and from 0.37 +/- 0.11 to 0.43 +/- 0.19; P = 0.1 respectively) with significant increase in left ventricular stroke volume (56 +/- 4 vs 9 +/- 5 %; P = 0.0013). S-NO-HSA compared to HSA treatment significantly improved ATP and PCr right ventricle myocardial content (13.9 +/- 1.1 vs. 7.0 +/- 1.8 and 5.9 +/- 3.3 vs. 1.9 +/- 0.6 micromol/g protein; P = 0.01) and increase tissue GSH/GSSG ratio (P = 0.001). CONCLUSIONS: S-NO-HSA reduces pulmonary hypertension and improves right ventricular diastolic function and right ventricular-arterial coupling with a positive effect on ventricular interdependence. This results in an increased energetic reserve of the heart and reduction of oxidative stress.

The “Missing” Link Between Acute Hemodynamic Effect and Clinical Response

The hemodynamic, mechanical and electrical effects of cardiac resynchronization therapy (CRT) occur immediate and are lasting as long as CRT is delivered. Therefore, it is reasonable to assume that acute hemodynamic effects should predict long-term outcome. However, in the literature there is more evidence against than in favour of this idea. This raises the question of what factor(s) do relate to the benefit of CRT. There is increasing evidence that dyssynchrony, presumably through the resultant abnormal local mechanical behaviour, induces extensive remodelling, comprising structure, as well as electrophysiological and contractile processes. Resynchronization has been shown to reverse these processes, even in cases of limited hemodynamic improvement. These data may indicate the need for a paradigm shift in order to achieve maximal long-term CRT response.

Mephedrone, a new designer drug of abuse, produces acute hemodynamic effects in the rat

Mephedrone (4-methylmethcathinone) is a new and popular drug of abuse widely available on the Internet and still legal in some parts of the world. Clinical reports are now emerging suggesting that the drug displays sympathomimetic toxicity on the cardiovascular system but no studies have yet explored its cardiovascular effects. Therefore we examined the effects of mephedrone on the cardiovascular system using a combination of in vitro electrophysiology and in vivo hemodynamic and echocardiographic measurements. Patch clamp studies revealed that mephedrone, up to 30 μM, had little effect on the major voltage-dependent ion channels of the heart or on action potentials recorded in guinea pig myocytes. Subcutaneous administration of mephedrone (3 and 15 mg/kg) to conscious telemetry-implanted rats produced dose-dependent increases in heart rate and blood pressure which persisted after pre-treatment with reserpine. Echocardiographic analysis demonstrated that intravenous injection of mephedrone (0.3 and 1 mg/kg) increased cardiac function, including cardiac output, ejection fraction, and stroke volume, similar to methamphetamine (0.3 mg/kg). We conclude that mephedrone is not directly pro-arrhythmic, but induces substantial increases in heart rate, blood pressure and cardiac contractility and this activity contributes to the cardiovascular toxicity in people who abuse the drug.

Baseline left ventricular dP/dtmax rather than the acute improvement in dP/dtmax predicts clinical outcome in patients with cardiac resynchronization therapy

The maximum rate of left ventricular (LV) pressure rise (dP/dt(max)) has been used to assess the acute haemodynamic effect of cardiac resynchronization therapy (CRT). We tested the hypothesis that LV dP/dt(max) predicts long-term clinical outcome after initiation of CRT. This was a retrospective observational multicentre study in 285 patients in whom dP/dt(max) was measured invasively following implantation of a CRT device. The minimum required follow-up was 1 year. We analysed the relationship between dP/dt(max) and time to the composite endpoint, consisting of all-cause mortality, heart transplantation (HTX), or LV assist device (LVAD) implantation within the first year of CRT. Thirty-four events occurred after a mean follow-up of 160 days (range 21-359). Patients with an event had lower dP/dt(max) than patients without an event both at baseline (705 ± 194 vs. 800 ± 222 mmHg/s, P= 0.018) and during CRT (894 ± 224 vs. 985 ± 244 mmHg/s, P= 0.033), but the acute increase in dP/dt(max) was similar in patients with and without an event (190 ± 133 vs. 185 ± 115 mmHg/s, P= n.s.). Left ventricular dP/dt(max)-level at baseline and during CRT both predicted the clinical outcome after adjustment for gender, aetiology and New York Heart Association class: hazard ratio (HR) 0.791 [95% confidence interval (CI) 0.658-0.950, P= 0.012] and HR 0.846 (95% CI 0.723-0.991, P= 0.038), respectively. Left ventricular dP/dt(max) measured at baseline and during CRT are predictors of 1-year survival free from all-cause mortality, HTX, or LVAD implantation, but the acute improvement in dP/dt(max) is not correlated to clinical outcome.

Tyrosine Kinase Inhibitors Are Potent Acute Pulmonary Vasodilators in Rats

Tyrosine kinase inhibitors are promising for the treatment of severe pulmonary hypertension. Their therapeutic effects are postulated to be due to inhibition of cell growth-related kinases and attenuation of vascular remodeling. Their potential vasodilatory activities have not been explored. Vasorelaxant effects of the tyrosine kinase inhibitors imatinib, sorafenib, and nilotinib were examined in isolated pulmonary arterial rings from normal and pulmonary hypertensive rats. Phosphorylation of myosin light chain phosphatase and myosin light chain was assessed by Western blots. Acute hemodynamic effects of imatinib were tested in the pulmonary hypertensive rats. In normal pulmonary arteries, imatinib reversed serotonin- and U46619-induced contractions in a concentration-dependent and endothelium-independent manner. Sorafenib and nilotinib relaxed U46619-induced contraction. Imatinib inhibited activation of myosin phosphatase induced by U46619 in normal pulmonary arteries. All three tyrosine kinase inhibitors concentration-dependently and completely reversed the spontaneous contraction of hypertensive pulmonary arterial rings unmasked by inhibition of nitric oxide synthase. Acute intravenous administration of imatinib reduced high right ventricular systolic pressure in pulmonary hypertensive rats, with little effect on left ventricular systolic pressure and cardiac output. We conclude that tyrosine kinase inhibitors have potent pulmonary vasodilatory activity, which could contribute to their long-term beneficial effect against pulmonary hypertension. Vascular smooth muscle relaxation mediated via activation of myosin light chain phosphatase (Ca(2+) desensitization) appears to play a role in the imatinib-induced pulmonary vasodilation.

Acute left ventricle diastolic function improvement after transcatheter aortic valve implantation

Data regarding the effects of TAVI on LV after are scarce and conflicting results have been reported immediately after aortic valvuloplasty. This study aimed to determine the acute haemodynamic effects of transcatheter aortic valve implantation (TAVI) in left ventricle (LV) diastolic performance, immediately after aortic valvuloplasty and prosthesis deployment. Sixty-one patients with severe aortic valve stenosis, and preserved LV systolic function submitted to successful TAVI, were included. All procedures were guided through transoesophageal echocardiography, and parameters of diastolic function were evaluated before and minutes after TAVI. The mean age was 83.5±6 years and mean log EuroSCORE was 18.2±9.4. Before the procedure, all patients presented LV diastolic dysfunction. Immediately after TAVI, fewer patients presented a restrictive pattern [27 (44.3%), before the procedure, vs. 20 (34.4%), after TAVI (P=0.047)], and an increase in E wave deceleration time (211.2±75.5 vs. 252.7±102.3 cm/s, P=0.001), in E wave velocity (109.5±41.2 vs. 120.3±43.6 cm/s, P=0.025), and in isovolumetric relaxation time (83±36.5 vs. 97.1±36.0 ms, P=0.013) was observed. On multivariate analysis of covariance (ANCOVA), adjusting to LV systolic function, heart rate, blood pressure, and haematocrit values, the results remained significant. Patients referred to percutaneous approach had invasive haemodynamic data collected, showing a decrease in LV end-diastolic pressure after valve implantation [18.8±5.7 vs. 14.7±4.7, mean difference -4.1 (95% CI: -5.9; -2.9)]. Patients with a restrictive pattern immediately after TAVI presented a smaller decrease in LV end diastolic pressure (-3.3±4.7) than those with diastolic dysfunction grade I or II (-9.5±4.7; P=0.017). This is the first study describing LV diastolic performance during TAVI. Our results show improvement in diastolic function parameters in patients with preserved LV systolic function, immediately after successful TAVI.

Acute haemodynamic effects of accelerated idioventricular rhythm in primary percutaneous coronary intervention

Accelerated idioventricular rhythm (AIVR) is very frequently observed in primary percutaneous coronary intervention (PCI), however knowledge of the haemodynamic effects is lacking. We studied an ST-segment elevation myocardial infarction cohort of 128 consecutive patients (aged 62±11 years) in whom AIVR occurred following reperfusion during primary PCI. Mean systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate were determined during periods of AIVR and sinus rhythm. We grouped patients according to the infarct-related artery and the site of the coronary occlusion. AIVR caused an immediate reduction in SBP (130±27 vs. 98±22 mmHg, p<0.001) and DBP (80±19 vs. 69±16 mmHg, p<0.001) and a small increase in heart rate (78±12 vs. 83±11 bpm, p<0.001) as compared to sinus rhythm, irrespective of infarct-related artery. Both absolute as well as relative reduction in SBP were more pronounced in distal than proximal left coronary artery (LCA) occlusions (36±16 vs. 27±12 mmHg, p<0.01, respectively 25±9 vs. 20±8%, p<0.05). These haemodynamic differences between proximal and distal occlusion sites were not observed in the right coronary artery. AIVR following reperfusion is associated with marked reduction in both SBP and DBP, irrespective of infarct-related artery. These haemodynamic effects are accompanied by only a very modest increase in heart rate during AIVR. Patients with a culprit lesion in the proximal LCA showed a smaller reduction in systolic blood pressure than distal LCA lesions.

Acute Hemodynamic Effects of Right and Left Ventricular Lead Positions during the Implantation of Cardiac Resynchronization Therapy Defibrillators

To evaluate the acute hemodynamic effects of different right (RV) and left ventricular (LV) pacing sites in patients undergoing the implantation of a cardiac resynchronization therapy defibrillator (CRT-D). Stroke volume index (SVI), assessed via pulse contour analysis, and dp/dt max, obtained in the abdominal aorta, were analyzed in 21 patients with New York Heart Association class III heart failure and left bundle branch block (mean ejection fraction of 24 ± 6%), scheduled for CRT-D implantation under general anesthesia. We compared the hemodynamic effects of RV apical (A), RV septal (B), and biventricular pacing using the worst (lowest SVI; C) and best (highest SVI; D) coronary sinus lead positions. Mean arterial pressure, SVI, and dp/dt max did not differ significantly between RV apical and septal pacing. Dp/dt max and SVI increased significantly during biventricular pacing (dp/dt max: B, 588 ± 160 mmHg/s; C, 651 ± 218 mmHg/s, P = 0.03 vs B; D, 690 ± 220 mmHg/s, P = 0.02 vs C; SVI: B, 33.6 ± 5.5 mL/m², C, 34.8 ± 6.1 mL/m², P = 0.08 vs B, D 36.0 ± 6.0 mL/m², P < 0.001 vs C). The best hemodynamic response was associated with lateral or inferior lead positions in 15 patients. Other LV lead positions were most effective in six patients. The optimal LV lead position varies significantly among patients and should be individually determined during CRT-D implantation. The impact of the RV stimulation site in patients with intraventricular conduction delay, undergoing CRT-D implantation, has to be investigated in further studies.

Extrasystolic stimulation with bi-ventricular pacing: an acute haemodynamic evaluation

Cardiac resynchronization therapy (CRT) by means of biventricular pacing (BiVP) is well established as a treatment for patients with heart failure (HF). Post-extrasystolic potentiation, (PESP) which involves a transient increase in myocardial contractility following a ventricular extrasystole, can be achieved using extrasystolic stimulation (ESS). On this basis, ESS has been proposed as a therapeutic. We assessed acute haemodynamic effects of ESS in the context of BiVP. Patients (n = 15, left ventricular ejection fraction < 40%, QRS ≥ 125 ms) with HF, received BiVP in combination with right ventricular (RV) ESS (single stimulus or pulse train). Left ventricular (LV) and peripheral arterial pressures were recorded and dP/dt was monitored. Addition of RV ESS to BiVP pacing led to a 21% increase in maximum (max) dP/dt (P < 0.001) and an 8.5 mm Hg increase in a systolic arterial pressure (P < 0.001). The modest fall in end-diastolic pressure (3.3 mmHg, P < 0.001) observed during ESS and BiVP was prevented by maintaining baseline sinus rate. Varying ESS modes or pacing outputs was not associated with differences in haemodynamic parameters. Biventricular pacing in combination with ESS, with maintenance of sinus rate, improves myocardial contractility in patients undergoing CRT.

SHA 026. Acute haemodynamic effect of atrio-biventricular pacing for patient undergoing coronary artery bypass graft surgery

SHA 026. Acute haemodynamic effect of atrio-biventricular pacing for patient undergoing coronary artery bypass graft surgery

100 Pressure vs flow as a guide for pacemaker optimisation? The acute haemodynamic effects of changes to atrioventricular delay

<h3>Background</h3> Non-invasive blood pressure monitoring by continuous finger photoplethysmography (Finometer) may have value in pacemaker optimisation. However, the immediate increment in blood pressure seems to diminish somewhat in the initial minute: it is unclear whether this is due to an (undesirable) fall in stroke volume or a (desirable) compensatory reduction in peripheral resistance. <h3>Methods and Results</h3> We studied this question by measuring beat-by-beat stroke volume (flow) using Doppler echocardiography, and blood pressure using continuous finger photoplethysmography, during and after atrioventricular delay adjustment from 40 to 120 ms in 19 subjects with cardiac pacemakers. Quintuplicate experimental runs were performed. Blood pressure and stroke volume (flow) both increased immediately (p&lt;0.00001 within one heartbeat). The immediate pressure increment correlated strongly with the immediate flow increment (r=0.74, p=0.0001). Pressure showed a partial decline a few seconds later (average rate 0.65 mm Hg/beat, r=–0.98, p&lt;0.0001), in contrast, flow did not decline (p=NS), Abstract 100 figure 1. Signal-to-noise ratio was significantly better for pressure than flow (6.3±3.6 vs 2.1±1.4, p&lt;0.0001), Abstract 100 figure 2. <h3>Conclusions</h3> Improving atrioventricular delay immediately increases blood pressure; however this effect decays slightly over the subsequent minute. This is due to compensatory vasodilatation rather than a reduction in cardiac function. Pressure changes are simpler to measure and easier to distinguish from random variation than Doppler measurements of flow, but are best measured immediately, before the vascular compensation.

The effects of anodal stimulation on electrocardiogram, left ventricular dyssynchrony, and acute haemodynamics in patients with biventricular pacemakers

Anodal stimulation (ANS) is a recognized phenomenon among patients with cardiac resynchronization therapy (CRT); this is noted during left ventricular (LV) pacing by the LV tip to right ventricular (RV) ring configuration. Its incidence varies according to the implanted hardware. We aim at evaluating the incidence of ANS and its acute haemodynamic effects among CRT patients. We screened all our patients who previously had an implanted CRT-P/D devices for ANS. After excluding all non-eligible devices, the initial screening was done by evaluating the programmer electrocardiogram (ECG) during device interrogation while pacing LV only from LV tip to RV ring. Those with ANS underwent screening by 12-lead ECG during biventricular pacing with VV interval programmed to 0. Patients with electrocardiographic evidence of ANS underwent detailed echocardiography. We screened 224 patients, 187 patients were excluded due to various causes. Thirty-seven subjects were analysed for this study. Anodal stimulation was found in 29 patients (78.4%) by primary screening. Twelve patients (41.4%) showed electrocardiographic evidence of ANS by 12-lead ECG. The ANS threshold was significantly higher than true bipolar LV threshold (4.5±1.7 vs. 1.1±0.3 V, respectively, P=<0.0001). Ten patients, with ECG evidence of ANS, underwent detailed echocardiography during biventricular pacing with and without ANS. Overall, there were no significant differences in the haemodynamic, echocardiographic, or resynchronization effects with and without ANS, two patients showed significant reduction in LV function with ANS. Anodal stimulation is a common phenomenon among CRT patients. In many cases ANS is seen with LV pacing only, while these changes may not be seen by ECG during biventricular pacing. Echocardiography did not show any significant acute haemodynamic benefit during ANS, and some patients may even deteriorate.

Acute Effects of Tobacco Chewing on the Systemic, Pulmonary and Coronary Circulation

Tobacco use is highly prevalent in India, with almost half of adult men consuming tobacco in either smoke or smokeless forms (particularly chewing). Although cigarette smoking is known to produce acute hemodynamic effects, there is a lack of data concerning such effects of chewing tobacco. The aim of this study was to determine the acute hemodynamic and coronary vasomotor effects of chewing tobacco. Twelve habitual tobacco chewers (mean ± SD age 51.3 ± 6.9 years) undergoing elective coronary angiography were included in the study. Following coronary angiography, a 7F thermodilution Swan Ganz continuous cardiac output pulmonary artery catheter was used to continuously measure the right heart pressures and cardiac output. Having obtained baseline hemodynamic data, 1g of tobacco was given to be chewed. Subsequently, hemodynamic data were obtained periodically over a period of 60 minutes. A repeat left coronary injection was performed, 10 minutes after giving the tobacco, in the right anterior oblique view to estimate the diameter of the left anterior descending (LAD) artery by quantitative coronary angiography. Chewing tobacco led to a significant acute increase in heart rate (from 68.3 ± 12.4 beats/min to 80.6 ± 14.6 beats/min, peaking at 10 minutes) and cardiac output (from 3.8 ± 0.45 L/min to 4.7 ± 0.64 L/min, peaking at 15 minutes). There were no significant changes in the right atrial, pulmonary artery, or wedge pressures and hence no change in the pulmonary vascular resistance. More importantly, chewing tobacco was associated with coronary vasoconstriction (proximal LAD diameter change from 3.17 ± 0.43 mm to 2.79 ± 0.37 mm; p-value 0.02; mid LAD diameter change from 2.75 ± 0.36 mm to 2.40 ± 0.22 mm; p-value 0.03). Chewing smokeless tobacco leads to coronary vasoconstriction and also produces significant hemodynamic alterations. These changes may have a bearing on excess vascular disease.

The Acute Hemodynamic Effects of MitraClip Therapy

The objective of this study was to evaluate the acute hemodynamic consequences of mitral valve (MV) repair with the MitraClip device (Abbott Vascular, Menlo Park, California). Whether surgical correction of mitral regurgitation (MR) results in a low cardiac output (CO) state because of an acute increase in afterload remains controversial. The acute hemodynamic consequences of MR reduction with the MitraClip device have not been studied. We evaluated 107 patients with cardiac catheterization before and immediately following percutaneous MV repair with the MitraClip device. In addition, pre- and post-procedural hemodynamic parameters were studied by transthoracic echocardiography. MitraClip treatment was attempted in 107 patients, and in 96 (90%) patients, a MitraClip was deployed. Successful MitraClip treatment resulted in: 1) an increase in CO from 5.0 ± 2.0 l/min to 5.7 ± 1.9 l/min (p = 0.003); 2) an increase in forward stroke volume (FSV) from 57 ± 17 ml to 65 ± 18 ml (p < 0.001); and 3) a decrease in systemic vascular resistance from 1,226 ± 481 dyn·s/cm(5) to 1,004 ± 442 dyn·s/cm(5) (p < 0.001). In addition, there was left ventricular (LV) unloading manifested by a decrease in LV end-diastolic pressure from 11.4 ± 9.0 mm Hg to 8.8 ± 5.8 mm Hg (p = 0.016) and a decrease in LV end-diastolic volume from 172 ± 37 ml to 158 ± 38 ml (p < 0.001). None of the patients developed acute post-procedural low CO state. Successful MV repair with the MitraClip system results in an immediate and significant improvement in FSV, CO, and LV loading conditions. There was no evidence of a low CO state following MitraClip treatment for MR. These favorable hemodynamic effects with the MitraClip appear to reduce the risk of developing a low CO state, a complication occasionally observed after surgical MV repair for severe MR.