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Background: Several wearable, medical-grade consumer ECG devices are now available and integrated into consumer electronics like multi sensor fitness watches and scales. Specific consumer ECGs can also come in the form of patches or thin sensor plates in credit card or other shapes. Watches with ECG capabilities are often multi vital sign sensor devices. The majority of these devices are usually connected to a mobile smartphone. However, there are pros and cons to their use., Methods: We review here an exemplary selection of modern consumer ECG devices based on device type, recording method and the number of standard ECG channels derived., Results: Single-channel consumer ECG devices such as Smart Watches can be useful for detecting and monitoring atrial fibrillation and flutter and other arrhythmias, as well as ectopic complexes. However, they are currently limited with respect to recording duration and information content (a single-channel or limb‑lead ECG having less diagnostic information than a 12‑lead ECG). While some non watch-based consumer ECG devices can now record all 6 limb leads to yield increased information, no consumer ECG devices can currently reliably detect ST-segment deviations, potentially indicating myocardial infarction or ischemic episodes. Moreover, barriers to use still exist for at-risk elderly people. Finally, there currently is no universal data exchange format., Conclusion: Consumer ECG devices, whether in fitness or fashionable design, allow for reliable detection of atrial fibrillation. Timely detection of atrial fibrillation and subsequent treatment might protect against stroke, especially in high-risk groups, yet prospective evidence is still lacking. Six-channel consumer ECG and longer data collection capabilities extend potential functionality, including for the monitoring of ST-segments and QT intervals. However, no currently available devices are sufficiently suitable for the detection of myocardial infarction or ischemia, which is why portable 12-channel technologies are desirable. For the reliable detection of a myocardial infarction, the determination of specific myocardial infarction blood markers and evaluation of patient medical history still is indispensable in addition to the 12 lead ECG., (Copyright © 2022. Published by Elsevier Inc.)

Objective: A recently developed immunoassay for high-sensitivity measurement of cardiac troponin T (hsTnT) allows measurement at the 99th percentile for a normal population with an assay imprecision <10%. It is unclear whether such a low cutpoint (14 ng/L) is helpful for long-term risk stratification of patients with an acute coronary syndrome (ACS) undergoing routine early invasive strategy., Patients and Main Outcome Measures: Consecutive patients with ACS admitted to a chest pain unit were studied. The usefulness of hsTnT for early diagnosis of myocardial infarction (MI) and prediction of all-cause death or death/MI over a median of 271 days following presentation was compared against the fourth generation cTnT at the 99th percentile cutpoint., Results: Of 1,384 patients with ACS enrolled, 47.8% had non-ST-segment elevation MI (NSTEMI), 26.4% unstable angina, 21.8% STEMI and 4% had non-ACS. Adjusted risk for all-cause death [adjusted HR 8.26 (95%CI: 1.13-66.33), p = 0.038] and death/MI [adjusted HR 2.71 (95% CI: 1.15-6.38), p = 0.023] were significantly higher with hsTnT above the 99th percentile. In particular, among patients with a standard fourth generation cTnT result below the 99th percentile cutoff (0.01 ng/mL), hsTnT improved risk assessment. Mortality risk associated with an elevated hsTnT was present across the spectrum of ACS, as well as in conditions with hsTnT elevations not related to ACS., Conclusion: hsTnT at the 99th percentile cutoff is useful for the diagnostic evaluation of patients with ACS, and provides strong and independent predictive power for adverse long-term outcomes even after early invasive strategy.

Aims: Objective methods for evaluating myocardial contrast echocardiography (MCE) are not yet widely available. We applied a Fourier analysis to myocardial contrast echocardiograms to identify myocardial perfusion defects., Methods: Harmonic power-Doppler contrast echocardiograms were performed in 21 patients undergoing Tl-201-SPECT imaging and in 13 controls. Images were transformed using Fourier analysis to obtain phase of the first harmonic sinusoidal curve displayed as color coded sequence of myocardial intensity changes. Means and standard deviations of regional phase angles were measured. The method was validated in an in vitro model. A contrast filled latex balloon was imaged at different gain settings mimicking defined time-intensity curves. An intraoperative porcine infarction model served to prove feasibility of Fourier transformation to analyze real-time pulse inversion contrast echocardiography., Results: In patients, phase imaging and intensity analysis showed focal areas with marked phase shifts (106 +/- 90 degrees) and heterogeneous distribution of phase angles (SD 66 +/- 17 degrees), correctly identifying 13/14 perfusion defects. The in vitro validation yielded increasing phase angles with increasing beta-values. This method was successfully applied to real-time MCE, identifying all infarction areas during occlusion of the left anterior descending artery., Conclusion: Phase analysis can be used to display dynamics of myocardial opacification.

The effects of intravenous ethmozine (3 mg.kg-1) on electrophysiological parameters of ischaemically damaged myocardium and induced ventricular tachyarrhythmias were studied by programmed stimulation in 17 conscious dogs with 4 to 8 day-old ligation of the left anterior descending coronary artery. Ethmozine showed a beneficial effect on sustained ventricular tachycardia by suppressing its inducibility in five of 14 animals or by slowing its rate in six of 14 animals. Ethmozine prolonged the ventricular effective refractory period in normal and infarcted myocardium, and impaired depressed conduction in ischaemically damaged tissue. The latter was indicated by significant lengthening of late potentials recorded from the infarction zone. The QT interval was only slightly increased with ethmozine. Our findings indicate an antiarrhythmic action of ethmozine in the late stage of myocardial infarction. Major mechanisms accounting for its efficacy may predominantly be associated with marked depression of slow conduction in the infarction zone, as well as with prolongation of ventricular refractoriness without significant changes of ventricular repolarization.

To evaluate the antiarrhythmic efficacy of l-sotalol and bisoprolol on inducible ventricular arrhythmias, conscious dogs with 4- to 8-day-old myocardial infarction were studied by programmed electrical stimulation. Direct recordings from infarcted and adjacent normal subepicardium were made using a specially designed composite electrode. From 18 dogs developing sustained ventricular tachycardia (sVT) during control stimulation, l-sotalol (1.5 mg/kg i.v.) prevented reinducibility of sVT in 10 animals, while in seven other animals it significantly reduced the rate of tachycardia. Bisoprolol (0.2 mg/kg i.v.), tested in a separate group of 10 dogs susceptible to sVT, was mostly ineffective in preventing or slowing the tachycardia. Both agents significantly prolonged conduction time and refractoriness within the atrioventricular conduction system, and decreased heart rate. However, while l-sotalol lengthened ventricular refractoriness and QT interval, bisoprolol exerted only a minor effect on these parameters. Neither of the drugs affected conduction in normal and infarcted myocardium, as indicated by almost unchanged QRS complex width and duration of ventricular late potentials, respectively. The results indicate that acute beta-blockade is ineffective against sVT induced during the subacute stage of myocardial infarction. The antiarrhythmic efficacy of l-sotalol may predominantly be related to its prolonging effect on ventricular refractoriness, supporting the concept of pure class III action.

The effects of prenylamine (PNL) and AQ-A 39 on sustained ventricular tachycardia (SVT) were studied by programmed stimulation in conscious dogs 4-10 days after ligation of the left anterior descending (LAD) coronary artery. In 8 of 16 dogs developing SVT in the control, PNL (3 mg/kg intravenously, i.v.) suppressed inducibility of SVT and slowed the rate of tachycardia in 6 other animals. In a separate group of 10 dogs with inducible SVT, AQ-A 39 (4 mg/kg i.v.) abolished elicitation of tachycardia in 3 dogs and decreased its rate in 6 other dogs. Neither drug affected normal conduction significantly, but PNL impaired slow conduction in the infarct zone, as indicated by prolongation of late potential. Both agents increased the effective refractory period (ERP) of infarcted and normal ventricular myocardium and prolonged the corrected QT interval. PNL and AQ-A 39 exert notable efficacy in preventing infarcted heart from severe ventricular arrhythmias. Prolongation of ventricular refractoriness and repolarization, as well as decreased slow conduction in ischemically damaged myocardium, are major mechanisms accounting for the effectiveness of these drugs against ventricular arrhythmias.

In recent years new methods of non-pharmacological therapy of ventricular tachyarrhythmias have gained increasing importance. The development of implantable defibrillators and increasing experience with catheter ablation techniques represent important alternatives to pharmacological antiarrhythmic therapy which is presently employed only in a subgroup of patients with life-threatening tachyarrhythmias and coronary heart disease.

In 12 anesthetized mongrel dogs (30 mg/kg pentobarbital), a thoracotomy was performed, and the left anterior descending coronary artery was ligated proximally. Eight to 12 days later, monophasic action potentials were recorded endocardially from the apex of the noninfarcted right ventricle and infarcted areas of the left ventricle, and the effects of 1.5 mg/kg intravenous sotalol were evaluated. Monophasic action potentials from the infarcted zone of the left ventricle were obtained from areas where fractionated bipolar electrograms could be recorded; this was histologically confirmed. After sotalol, in sinus rhythm, the monophasic action potential duration at 90% repolarization of the infarcted zone increased from 186 +/- 31 to 226 +/- 45 ms (+ 22%, p less than 0.05), and monophasic action potential duration of the noninfarcted zone increased from 184 +/- 31 to 225 +/- 47 ms (+ 22%, p less than 0.05). Programmed ventricular stimulation was performed with single extrastimuli at a basic drive cycle length of 300 ms. With long coupling intervals (290 ms), monophasic action potential duration of the infarcted zone increased from 165 +/- 23 to 183 +/- 25 ms (+ 11%, p less than 0.05) after sotalol; and monophasic action potential duration of the noninfarcted zone increased from 159 +/- 20 to 180 +/- 25 ms (+ 13%, p less than 0.05). With short coupling intervals (200 ms), the monophasic action potential duration of the noninfarcted zone increased from 157 +/- 19 to 173 +/- 18 ms (+ 10%, p less than 0.05), and monophasic action potential duration of the noninfarcted zone increased from 150 +/- 18 to 157 +/- 18 ms (+ 5%, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Study Objective: The aim was to characterise monophasic action potentials recorded from subacutely infarcted myocardial regions, where fractionated bipolar electrograms could be obtained., Design: Dogs underwent ligation of the left anterior descending coronary artery. Before and 8-12 d after ligation, monophasic action potentials and local electrograms were recorded endocardially from the apex of the left ventricle., Experimental Material: 15 anaesthetised mongrel dogs (30 mg pentobarbitone.kg-1) were used., Measurements and Main Results: Multiphasic fractionated bipolar electrograms could be recorded from infarcted sites of the left ventricle with a mean duration of 69(SD 10) ms and a mean amplitude of 3.7(1.6) mV, compared to control values of 42(7) ms (p less than 0.05) and 9.4(2.2) mV (p less than 0.05), respectively. Endocardial monophasic action potentials recorded from these areas were similar to action potentials obtained from non-infarcted sites before coronary ligation. The fractionated extracellular potentials were superimposed on the monophasic action potential upstroke. MAP90 was 189(31) ms, MAP30 138(12) ms, versus control values of 182(27) ms and 139(10) ms (NS). Monophasic action potential amplitude was significantly reduced at infarcted sites compared to control, at 26(7) mV v 38(6) mV. Histological specimens were taken to confirm that measurements were obtained from infarcted tissue., Conclusions: It is possible to record monophasic action potential in subacutely infarcted canine ventricular myocardium; this technique might help in further studies to characterise electrophysiological mechanisms of ventricular arrhythmias in chronic myocardial infarction in man.