Cardiac Arrest in Acute Myocardial Infarction: Concept of Circulatory Support With Mechanical Chest Compression and Impella to Facilitate Percutaneous Coronary Intervention.

Cardiogenic shock in the context of acute ST-elevation myocardial infarction (STEMI) remains a challenge to manage and results in significant mortality and morbidity, cardiac arrest in this setting even more so. The increase in myocardial oxygen demand and consumption with the use of inotropes is recognised as increasing mortality. Alternatives include the intra-aortic balloon pump (IABP), which has yet to be shown to improve outcomes, and extracorporeal membrane oxygenation (ECMO), which requires super-specialised techniques not widely available. We report a case of Anterior STEMI from a left main stem occlusion suffering with cardiac arrest on reaching the catheter laboratory table necessitating external mechanical compression with an Autopulse™. The patient remained in pulseless electrical activity (PEA) throughout, and was Autopulse dependent despite successful percutaneous coronary intervention (PCI). An Impella® was inserted for additional mechanical support and facilitated successful weaning from cardiopulmonary resuscitation (CPR). Despite 105minutes without a spontaneous output, we describe the first documented case of simultaneous use of Impella with mechanical CPR with a successful outcome; demonstrating a potential technique of good mechanical haemodynamic support to aide early revascularisation that may have potential utility in the treatment of cardiogenic shock and arrest.

To Revascularise or Not To Revascularise, That Is the Question: the Diagnostic and Management Conundrum of Ischaemic Cardiomyopathy.

Ischaemic cardiomyopathy is an important cardiovascular condition that has differing pathophysiological substrates and clinical manifestations. Contemporary management involves the administration of heart failure pharmacotherapy and device therapy where indicated, which has good prognostic data to support it. Whilst the role of revascularisation is clear in those patients presenting with an acute coronary syndrome or angina, the role in those patients presenting either incidentally, with predominant heart failure symptoms, or in those presenting with acute heart failure with an associated elevated troponin is less well defined and lacks randomised outcome data to support its adoption. The aim of this review is therefore to discuss the challenges in the diagnosis of ischaemic cardiomyopathy with a review of the existing imaging modalities that can facilitate, and to revisit the variety of clinical presentations that can occur, with particular emphasis on the contemporary role of revascularisation in these cohorts of patients.

Coronary Jeopardy Score Predicts Ischemic Etiology in Patients With Left Ventricular Systolic Dysfunction.

While cardiovascular magnetic resonance imaging (CMR) is the gold standard diagnostic test for heart failure etiology, it is not universally available. Our aim was to investigate whether quantifying the extent of coronary disease on angiography can predict the presence of an ischemic etiology. We included 176 patients who underwent CMR and coronary angiography for new heart failure with reduced ejection fraction. Based on CMR, 65% had an ischemic etiology and 35% were non-ischemic. A BCIS jeopardy score threshold ≥6 had 76% sensitivity and 97% specificity. In HFrEF, the extent of coronary disease on angiography can be used to rule in or out an ischemic etiology.

The physiological effects of cardiac resynchronization therapy on aortic and pulmonary flow and dynamic and static components of systemic impedance.

BACKGROUND: Patients who improve following cardiac resynchronization therapy (CRT) have left ventricular (LV) remodeling and improved cardiac output (CO). Effects on the systemic circulation are unknown. OBJECTIVE: To explore the effects of CRT on aortic and pulmonary blood flow and systemic afterload. METHODS: At CRT implant patients underwent a noninvasive assessment of central hemodynamics, including wave intensity analysis (n = 28). This was repeated at 6 months after CRT. A subsample (n = 11) underwent an invasive electrophysiological and hemodynamic assessment immediately following CRT. CRT response was defined as reduction in LV end-systolic volume ≥15% at 6 months. RESULTS: In CRT responders (75% of those in the noninvasive arm), there was a significant increase in CO (from 3 ± 2 L/min to 4 ± 2 L/min, P = .002) and LV dP/dtmax (from 846 ± 162 mm Hg/s to 958 ± 194 mm Hg/s, P = .001), immediately after CRT in those in the invasive arm. They demonstrated a significant increase in aortic forward compression wave (FCW) both acutely and at follow-up. The relative change in LV dP/dtmax strongly correlated with changes in the aortic FCW (R s 0.733, P = .025). CRT responders displayed a significant reduction in afterload, and a decrease in systemic vascular resistance and pulse wave velocity acutely; there was a significant decrease in acute pulmonary afterload measured by the pulmonary FCW and forward expansion wave. CONCLUSION: Improved cardiac function following CRT is attributable to a combination of changes in the cardiac and cardiovascular system. The relative importance of these 2 mechanisms may then be important for optimizing CRT.

Impact of coronary artery disease on contractile function and ventricular-arterial coupling during exercise: Simultaneous assessment of left-ventricular pressure-volume and coronary pressure and flow during cardiac catheterization.

Coronary artery disease (CAD) can adversely affect left ventricular (LV) performance during exercise by impairment of contractile function in the presence of increasing afterload. By performing invasive measures of LV pressure-volume and coronary pressure and flow during exercise, we sought to accurately measure this with comparison to the control group. Sixteen patients, with CCS class >II angina and CAD underwent invasive simultaneous measurement of left ventricular pressure-volume and coronary pressure and flow velocity during cardiac catheterization. Measurements performed at rest were compared with peak exercise using bicycle ergometry. The LV contractile function was measured invasively using the end-systolic pressure-volume relationship, a load independent marker of contractile function (Ees). Vascular afterload forces were derived from the ratio of LV end-systolic pressure to stroke volume to generate arterial elastance (Ea). These were combined to assess cardiovascular performance (ventricular-arterial [VA] coupling ratio [Ea/Ees]). Eleven patients demonstrated flow-limiting (FL) CAD (hyperemic Pd/Pa <0.80; ST-segment depression on exercise); five patients without flow-limiting (NFL) CAD served as the control group. Exercise in the presence of FL CAD was associated impairment of Ees, increased Ea, and deterioration of VA coupling. In the control cohort, exercise was associated with increased Ees and improved VA coupling. The backward compression wave energy directly correlated with the magnitude contraction as measured by dP/dTmax (r = 0.88, p = 0.004). This study demonstrates that in the presence of flow-limiting CAD, exercise to maximal effort can lead to impairment of LV contractile function and a deterioration in VA coupling compared to a control cohort.

Physiological Impact of Afterload Reduction on Cardiac Mechanics and Coronary Hemodynamics Following Isosorbide Dinitrate Administration in Ischemic Heart Disease.

Understanding the cardiac-coronary interaction is fundamental to developing treatment strategies for ischemic heart disease. We sought to examine the impact of afterload reduction following isosorbide dinitrate (ISDN) administration on LV properties and coronary hemodynamics to further our understanding of the cardiac-coronary interaction. Novel methodology enabled real-time simultaneous acquisition and analysis of coronary and LV hemodynamics in vivo using coronary pressure-flow wires (used to derive coronary wave energies) and LV pressure-volume loop assessment. ISDN administration resulted in afterload reduction, reduced myocardial demand, and increased mechanical efficiency (all P<0.01). Correlations were demonstrated between the forward compression wave (FCW) and arterial elastance (r=0.6) following ISDN. In the presence of minimal microvascular resistance, coronary blood flow velocity exhibited an inverse relationship with LV elastance. In summary this study demonstrated a reduction in myocardial demand with ISDN, an inverse relationship between coronary blood flow velocity and LV contraction-relaxation and a direct correlation between FCW and arterial elastance. The pressure volume-loop and corresponding parameters b The pressure volume loop before (solid line) and after (broken line) Isosorbide dintrate.

The molecular phenotype of human cardiac myosin associated with hypertrophic obstructive cardiomyopathy.

AIM: The aim of the study was to compare the functional and structural properties of the motor protein, myosin, and isolated myocyte contractility in heart muscle excised from hypertrophic cardiomyopathy patients by surgical myectomy with explanted failing heart and non-failing donor heart muscle. METHODS: Myosin was isolated and studied using an in vitro motility assay. The distribution of myosin light chain-1 isoforms was measured by two-dimensional electrophoresis. Myosin light chain-2 phosphorylation was measured by sodium dodecyl sulphate-polyacrylamide gel electrophoresis using Pro-Q Diamond phosphoprotein stain. RESULTS: The fraction of actin filaments moving when powered by myectomy myosin was 21% less than with donor myosin (P = 0.006), whereas the sliding speed was not different (0.310 +/- 0.034 for myectomy myosin vs. 0.305 +/- 0.019 microm/s for donor myosin in six paired experiments). Failing heart myosin showed 18% reduced motility. One myectomy myosin sample produced a consistently higher sliding speed than donor heart myosin and was identified with a disease-causing heavy chain mutation (V606M). In myectomy myosin, the level of atrial light chain-1 relative to ventricular light chain-1 was 20 +/- 5% compared with 11 +/- 5% in donor heart myosin and the level of myosin light chain-2 phosphorylation was decreased by 30-45%. Isolated cardiomyocytes showed reduced contraction amplitude (1.61 +/- 0.25 vs. 3.58 +/- 0.40%) and reduced relaxation rates compared with donor myocytes (TT(50%) = 0.32 +/- 0.09 vs. 0.17 +/- 0.02 s). CONCLUSION: Contractility in myectomy samples resembles the hypocontractile phenotype found in end-stage failing heart muscle irrespective of the primary stimulus, and this phenotype is not a direct effect of the hypertrophy-inducing mutation. The presence of a myosin heavy chain mutation causing hypertrophic cardiomyopathy can be predicted from a simple functional assay.

Mechanical Circulatory Support in the Cardiac Catheterization Laboratory for Cardiogenic Shock.

Despite the development of acute revascularisation, the mortality rate for cardiogenic shock remains around 50%. Mechanical circulatory support devices have long held promise in improving outcomes in shock, but high-quality evidence of benefit has not been forthcoming. In this article we review the currently available devices for treating shock, their physiological effects and the evidence base for their use in practice. We subsequently look ahead within this developing field, including new devices and novel indications for established technology.

Intra-aortic Balloon Counterpulsation for High-Risk Percutaneous Coronary Intervention: Defining Coronary Responders.

The effect of intra-aortic balloon counterpulsation (IABC) varies, and it is unknown whether this is due to a heterogeneous coronary physiological response. This study aimed to characterise the coronary and left ventricular (LV) effects of IABC and define responders in terms of their invasive physiology. Twenty-seven patients (LVEF 31 ± 9%) underwent coronary pressure and Doppler flow measurements in the target vessel and acquisition of LV pressure volume loops after IABC supported PCI, with and without IABC assistance. Through coronary wave intensity analysis, perfusion efficiency (PE) was calculated as the proportion of total wave energy comprised of accelerating waves, with responders defined as those with an increase in PE with IABC. The myocardial supply/demand ratio was defined as the ratio between coronary flow and LV pressure volume area (PVA). Responders (44.4%) were more likely to have undergone complex PCI (p = 0.03) with a higher pre-PCI disease burden (p = 0.02) and had lower unassisted mean arterial (87.4 ± 11.0 vs. 77.8 ± 11.6 mmHg, p = 0.04) and distal coronary pressures (88.0 ± 11.0 vs. 71.6 ± 12.4 mmHg, p < 0.001). There was no effect overall of IABC on the myocardial supply/demand ratio (p = 0.34). IABC has minimal effect on demand, but there is marked heterogeneity in the coronary response to IABC, with the greatest response observed in those patients with the most disordered autoregulation.